Yuchuan Zhou
Zhonghui Jiang2
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- 1Department of Oncology, Affiliated Hospital of North Sichuan Medical College, Nanchong, China
- 2Thoracic Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, China
Collagen comprises approximately 30% of the body’s protein content and is essential for maintaining the structural integrity, support, and strength of the skin, muscles, bones, and connective tissues. Recent research has further elucidated its role in various aspects of tumor biology, including tumorigenesis, invasion, migration, drug resistance, and recurrence. Furthermore, collagen is involved in prognostic assessments, the evaluation of therapeutic efficacy, immunoregulation, and the identification of potential treatment targets in oncology. This review examines a range of tumor types, including lung, gastric, breast, melanoma, and colorectal cancers, among others. Our objective is to differentiate these tumors based on the specific types of collagen present and to analyze the roles of various collagen types in tumor development, progression, prognosis, and their potential as therapeutic targets.
1 Introduction
Collagen, a fundamental component of the extracellular matrix (ECM), is ubiquitously distributed across various organs and tissues, playing a crucial role in maintaining the structural integrity of the ECM (1, 2). To date, 28 distinct collagen types have been identified, each differing in molecular structure, associated cellular components, and specific anatomical distribution (3). Collagen is predominantly secreted by fibroblasts, myoblasts, adipocytes, endothelial cells, and certain epithelial cells, and is vital for wound healing and tissue repair due to its capacity to facilitate cell migration and proliferation (4–7). Furthermore, collagen acts as a signaling molecule, regulating a wide array of cellular processes, including differentiation, modulation of inflammatory responses, immune function, and gene expression, thereby contributing to the maintenance of overall physiological homeostasis (8–15).
Clinical evidence indicates that chemotherapy and immunotherapies exhibit significantly diminished efficacy in treating solid tumors compared to hematological malignancies (16, 17). These findings highlight the distinct role of the tumor microenvironment (TME) in reducing therapeutic effectiveness in solid tumors. Collagen is a pivotal component of the TME. A diverse array of cell types, including cancer cells, cancer-associated fibroblasts (CAFs), endothelial cells, and immune cells, contributes substantially to collagen synthesis (18). These cells produce procollagen, which is subsequently secreted into the ECM and processed by proteases into mature collagen fibers (19). Collagen is the primary determinant of the density and stiffness of the TME and has been implicated in tumorigenesis, progression, invasion, metastasis, drug resistance, and immunoregulation (20–24). Additionally, alterations in collagen organization within the tumor microenvironment have been associated with prognostic outcomes. Changes in collagen characteristics—such as content, maturity, morphology, and architecture—have been correlated with prognosis, indicating that collagen width may serve as a significant prognostic marker (25–29).
Strategies targeting collagen depletion have been proposed to enhance drug delivery in solid tumors. In particular, collagen depletion has been explored as a strategy to improve drug delivery and increase the effectiveness of phototherapy in pancreatic cancer (30–32). Moreover, its potential impact on modulating the efficacy of immunotherapy has been relatively understudied. Recent advancements in the investigation of the ECM have highlighted the role of collagen in promoting an immunosuppressive TME and serving as a physical barrier that protects tumors from immunotherapy (33, 34). Additionally, research has shown that tumor-associated macrophages contribute to the progression of bladder tumors by secreting Type I collagen, which subsequently activates the pro-survival PI3K/AKT signaling pathway (35). Furthermore, changes in collagen have been examined in relation to postoperative anastomotic stenosis following neoadjuvant chemoradiotherapy for rectal cancer.
This review aims to deliver an exhaustive analysis of the recent roles of various collagen types across different tumor classifications, thereby establishing a foundation for personalized and precise tumor therapies.
2 The role of collagen types in tumors and current treatment methods
2.1 Type I collagen
COL1 is the most prevalent member of the collagen family, predominantly located in tissues such as skin, bones, muscles, and blood vessels. It plays a critical role in wound healing and tissue regeneration. In the context of cancer, COL1 is often associated with tumor progression and aggressiveness, COL1 mainly secreted by CAF and significantly contributes to the TME, It not only impedes the infiltration of tumor-immune cells and therapeutic agents via mechanical forces but also enhances tumor growth through intermolecular interactions across various tumor types (36–41). COL1 supports glioblastoma stem cells (GSCs) by enhancing CD133-p85 interaction and Akt phosphorylation. This boosts ATF4 protein levels, increasing SLC1A5-dependent glutamine uptake and glutathione synthesis, thereby promoting GSC self-renewal and tumor growth (42). On the contrary, research indicates that COL1-mediated tumor suppression counteracts the tumor-promoting effects ofCAF, underscoring the complex interactions within the tumor stroma (43, 44). COL1 also possesses prognostic value in cancers such as gastric, colorectal, and breast cancer (45, 46), particularly serving as an independent predictor of 5-year overall survival and recurrence-free survival in patients with TNM stage II/III colorectal cancer undergoing surgical treatment (47).
The abundant presence of COL1 facilitates its deposition and cross-linking, resulting in the formation of a rigid and dense physical barrier. This barrier restricts drug penetration and immune cell infiltration, thereby contributing to drug resistance and metabolic adaptations. Consequently, COL1 has been identified as a therapeutic target in cancer treatment, with approaches such as collagenase treatment, protein-free collagen degradation, collagen-degrading bacteria, and the degradation of the tumor extracellular matrix mediated by armed oncolytic viruses, all demonstrating significant efficacy (48–51). Furthermore, the status of collagen crosslinking is a significant determinant of tissue stiffness. This can be influenced by modulating the enzymatic activity of lysyl oxidase and altering collagen glycation-related crosslinking (52, 53). Additionally, there is growing interest in repurposing approved antifibrotic medications, which target collagen synthesis and maturation, as anticancer drugs. For example, halofuginone, an antifibrotic agent, inhibits the activation of Smad3 in fibroblasts in response to transforming growth factor beta (TGF-β1) stimulation. COL1 contains collagen-binding domains (CBD), which can be utilized in the engineering of antibodies, drugs, or cytokines. Incorporating a CBD into these therapeutic agents facilitates their targeted delivery and release within the tumor collagen scaffold. This approach minimizes off-target effects, reduces systemic toxicity, and enhances localized retention, thereby improving therapeutic efficacy. Additionally, COL1 is implicated in various facets of cancer biology. For instance, the mineralization of COL1 influences the glycocalyx of breast cancer cells, potentially affecting NK cell-mediated cytotoxicity (54). Studies have identified a homotrimer COL1 signature linked to clinical manifestations and tertiary lymphoid structures in liver cancer (55). Furthermore, a COL1-specific imaging probe has been utilized to assess treatment response in pancreatic cancer, underscoring the role of tumor-associated fibrosis in disease progression (56). Moreover, COL1 has been associated with apoptotic balance in hepatocellular carcinoma cells, highlighting the complex interplay between collagen types and apoptotic responses in cancer (57). Modulating STAT3 signaling in COL1-positive fibroblasts presents a promising strategy for managing colitis-associated cancer, highlighting the therapeutic potential of targeting collagen-expressing fibroblasts in oncological treatments. Collectively, these studies emphasize the critical role of COL1 in tumor biology and its interactions with stroma cells, offering valuable insights into potential diagnostic, prognostic, and therapeutic applications across various cancer types.
2.2 Type III collagen
COL3 is the second most prevalent collagen in tissues and is frequently co-expressed with COL1, also secreted by CAF. Notably, COL3 primarily functions as a tumor suppressor and serves as a prognostic marker. Previous studies have suggested that a collagen-rich peritumoral stroma, particularly rich in COL3, may adversely affect the interaction between T cells and tumor cells. This interaction can lead to immune exclusion and potential resistance mechanisms in patients with metastatic melanoma following PD-1 inhibition (58). Furthermore, COL3 has been demonstrated to exert a tumor-restrictive effect in human breast cancer. In biopsy samples of human triple-negative breast cancer, a study reveals an increased deposition of COL3 compared to COL1 in non-invasive regions as opposed to invasive regions. Correspondingly, a bioinformatics analysis of over 1,000 breast cancer patient biopsies from The Cancer Genome Atlas BRCA cohort indicates that patients exhibiting higher COL3:COL1 expression ratios in bulk tumor samples experience enhanced overall, disease-free, and progression-free survival compared to those with elevated COL1:COL3 expression ratios (59). In a similar vein, recombinant humanized COL3 has been shown to inhibit ovarian cancer and induce protective anti-tumor immunity by modulating autophagy through GSTP1 (60).
Furthermore, dormant cancer cells establish an ECM niche enriched with COL3, which interacts with discoidin domain receptor 1 (DDR1) to induce and maintain cellular dormancy (61). The differential expression of COL3A1 in human cancer tissues compared to normal samples underscores its positive correlation with tumor-infiltrating immune cells (62). A recent review has discussed the prognostic value of quantifying tumor fibrosis by measuring the pro-peptide of COL3 in serum across various solid tumor types, highlighting its significance in understanding prognosis and guiding future drug development efforts (63). An enzyme-linked immunosorbent assay (ELISA) targeting a circulating COL3 fragment, derived from fibroblast activation protein (FAP) cleavage, has been developed to reflect FAP activity in patients with non-small cell lung cancer and spondyloarthritis (64). Additionally, keloid-like collagen, which contains both COL3 and COL1, has been evaluated for its diagnostic and prognostic significance in the remodeling patterns of the extracellular matrix in colorectal cancer, emphasizing the importance of quantitative visual assessment in determining prognosis (47). Furthermore, digital whole slide image analysis was employed using COL3 to assess the prognostic significance of stromal markers in triple-negative breast cancer (46). In conclusion, COL3 seems to have a substantial impact on tumor biology, influencing diagnosis, prognosis, and therapeutic approaches across different cancer types. Further investigation into the interactions between COL3 and tumors is necessary to enhance our understanding of its potential as a target for cancer treatment.
2.3 Type IV collagen
COL4, a key component of the basement membrane (BM), is critically involved in tumor progression and therapeutic response. COL4 has been shown to facilitate malignant cell proliferation. Three-dimensional (3D) biomimetic cell culture platforms utilizing COL4 pre-treated hydrogels have been found to support the proliferation of glioblastoma cells (65). One study assessed COL4 levels in patients with clear cell renal cell carcinoma (ccRCC) and proposed that variations in COL4 concentrations may contribute to malignant tumor progression (66). Another study explored the association between COL4 and hepatocellular carcinoma (HCC) prognosis in patients undergoing hepatectomy, indicating a potential link between COL4 levels and HCC malignant behaviors (67). Conversely, it has been demonstrated that activated T-cells release granzyme B (GzB), which can cleave type IV collagen during tumor infiltration. This finding suggests that measuring GzB-generated type IV collagen degradation fragments in liquid biopsies could be useful for identifying metastatic melanoma patients who are responding to immune checkpoint inhibitor therapy (58). Furthermore, the α4 NC1 domain of type IV collagen, referred to as Tetrastatin, has been demonstrated to inhibit tumor growth in a mouse melanoma model by attenuating VEGF-induced angiogenesis (68). In the context of breast cancer, type IV collagen has been associated with tumor progression and the regulation of metabolism. The α5 chain of type IV collagen is predominantly expressed in luminal-type breast cancer and is regulated by estrogen receptor-α, functioning as a microenvironmental regulator that influences cancer cell metabolism (69). Additionally, stromal expression of COL4 has been recognized as a prognostic indicator in small invasive breast cancers (70). Collectively, COL4 and its degradation products are integral to tumor biology, immune response, and therapeutic outcomes across various cancer types, including melanoma and breast cancer. Elucidating the interactions between COL4 and the TME may offer valuable insights for the development of innovative therapeutic strategies and biomarkers for cancer diagnosis and treatment monitoring.
2.4 Type VI collagen
COL6 establishes a filamentous network within connective tissue, facilitating the linkage between matrix macromolecules and cells. It interacts with COL5 and fibronectin, thereby enhancing the structural integrity of tissue scaffolds. Additionally, COL6 plays a crucial role in mediating cell adhesion and promoting cellular migration. COL6 has been implicated in various aspects of tumor progression and metastasis. In breast cancer research, it has been discovered that oncogenic linear COL6 in invasive breast cancer is induced by CCL5, suggesting a potential role in the disease’s progression (71). Similarly, it has been demonstrated that COL6 regulates the CDK4/6-p-Rb signaling pathway, thereby promoting ovarian cancer invasiveness, stemness, and metastasis (72). Additionally, COL6 deposition primes the glioblastoma microenvironment for invasion through mechanostimulation of β-catenin signaling. Conversely, a study indicated that COL6-α1 and COL6-α2 suppress the proliferation, migration, and invasion of bladder cancer cells, highlighting the complex role of collagen VI in different cancer types (73).
Through the application of machine learning techniques, researchers identified epithelial-mesenchymal transition (EMT)-related genes associated with cervical cancer etiology and prognosis, with COL6 emerging as a potential prognostic indicator in cervical cancer (74). Additionally, a study constructed a reliable five-gene prognostic signature for colon adenocarcinoma associated with the wild-type allelic state of the COL6A6 gene (75). By identifying independent prognostic signatures based on allelic variations, the researchers elucidated significant prognostic disparities between high-risk and low-risk patient cohorts. This finding implies that the genetic context associated with collagen genes may influence cancer prognosis. Furthermore, a study demonstrated that sarcoma cells secrete hypoxia-modified COL6, which compromises the integrity of the lung endothelial barrier and facilitates metastasis, thereby indicating a direct involvement of COL6 in promoting cancer cell migration and invasion (76). Additionally, research has shown that immune cells contribute to the dynamics of mammary collagen during pregnancy, suggesting a potential connection between collagen regulation and immune responses within the tumor microenvironment (77). In conclusion, investigations into COL6 and its interactions with tumors underscore.
2.5 Type X collagen
COL10 is a relatively understudied collagen type in the context of cancer, particularly when compared to other collagen types such as types I, III, and V. Nonetheless, recent research has begun to elucidate the potential role of COL10 in cancer progression. The COL10 α1 chain (COL10A1), which encodes the α−1 chain of COL10, plays a crucial role in providing tensile strength and structural integrity to tissues. The upregulation of COL10A1 has been shown to facilitate the progression of triple-negative breast cancer through the Wnt/β-catenin signaling pathway (78). In colorectal, prostate, pancreatic, and gastric cancers, COL10A1 is associated with poor prognosis and is linked to tumor vasculature (79–85). Furthermore, COL10 has been found to facilitate prostate cancer progression by interacting with INHBA to activate the PI3K/AKT pathway (81). Additionally, stromal COL10A1 and tumor-infiltrating lymphocytes have been identified as potential predictive markers for neoadjuvant therapy in estrogen receptor-positive/HER2-positive breast cancer (86, 87).The COL10A1 gene facilitates the stratification of colon cancer invasiveness and is associated with the enrichment of the extracellular matrix and immune cells within the tumor parenchyma (88). Furthermore, the secretion of COL10A1 in lung cancer cells promotes metastasis and attracts cancer-associated fibroblasts (89). Additionally, miR-384 induces apoptosis and autophagy in non-small cell lung cancer cells by negatively regulating the COL10A1 gene (90).
2.6 Type XI collagen
COL11 has been implicated in various tumor types, particularly osteochondrogenic tumors (91). The expression of COL2 and COL11 has been observed in canine mammary mixed tumors, where tumor cells exhibited collagen production in collagen gel culture (92). A related study demonstrated that COL11A1-regulated hypermethylation leads to the downregulation of miR-509-3p expression, thereby facilitating cancer progression and chemoresistance in ovarian cancer cells. This research elucidates the complex mechanisms involving COL11A1 in cancer progression (93). Furthermore, COL11 has been identified as a potential biomarker in cancer research, with noninvasive biomarkers targeting the propeptides of the COL11 alpha-1 chain (PRO-C11) being developed for patients with pancreatic ductal adenocarcinoma, enabling the quantification of COL11 production (94, 95). Additionally, COL11 was found to be significantly upregulated in lung adenocarcinoma tissues compared to non-tumor tissues, suggesting its potential involvement in this type of cancer (96). Furthermore, the interaction between COL11 and tumor cells has been investigated within the framework of lung cancer. COL11 has been shown to inhibit the functions of lung cancer-associated fibroblasts and limit the availability of integrin binding sites on the COL1 matrix, suggesting its potential role in modulating the tumor microenvironment (97). The existing literature indicates that COL11 may play a crucial role in tumorigenesis and could serve as a valuable biomarker for cancer diagnosis and prognosis. Additional research is required to elucidate the specific mechanisms by which COL11 is involved in various tumor types.
2.7 Type XVII collagen
COL17, also referred to as BP180, along with integrin α6β4, CD151, plectin, and BP230, constitutes essential components of type I hemidesmosomes (HDs). These components play a pivotal role in mediating interstitial adhesion, facilitating cell polarization, and maintaining the spatial organization of tissue architecture. Furthermore, COL17 is significantly implicated in various aspects of tumor biology. Notably, it has been shown to regulate tumor growth in pancreatic and colorectal cancers (20). Specifically, COL17 promotes the dormancy of colorectal cancer cells by activating mTORC2 signaling (98). Conversely, it has been reported that COL17 inhibits the proliferation and growth of breast cancer cells through the deactivation of the AKT/mTOR signaling pathway (99). Additionally, a study indicated that elevated levels of the ectodomain of COL17 in circulation serve as a prognostic marker for patients with metastatic colorectal cancer, suggesting that PRO-C17 could be utilized as a non-invasive biomarker to elucidate tumor heterogeneity and its role in tumor progression (100). Similarly, type COL17 collagen may serve as a tumor biomarker in head and neck squamous cell carcinoma. A study has highlighted the tissue-specific expression of type COL17 isoforms and their molecular interactions with P120 catenin, underscoring their role in epidermal keratinocyte cell-cell adhesion (101). Furthermore, COL17 has been identified as a potential target for fluorescence-guided surgery in non-small cell lung cancers, highlighting its significance as a cell surface biomarker in tumor tissues (102). Collectively, these studies emphasize the critical role of type COL17 collagen in tumor biology and its potential as a prognostic marker across various cancer types.
2.8 Other types of collagen associated with cancer
The literature on COL5, COL7, COL9, and COL12 in the context of tumors is limited, with only a few studies addressing their functions and roles as tumor markers. Consequently, numerous functions and underlying mechanisms remain poorly understood.
Type V collagen (COL5) is a regulatory fibril-forming collagen that plays a relatively minor role within the ECM. COL5 is synthesized in various mesenchymal cells and its gene expression is modulated by TGF-β and growth factors (105). Morphologically, COL5 is incorporated into heterotypic fibrils in conjunction with COL1. In the context of oncogenesis, myofibroblast-derived COL5 contributes to elevated mechanical stress within tissues, thereby promoting metastasis and resistance to therapy in lung adenocarcinoma cells (106). Additionally, COL5A1 has been implicated in the progression of triple-negative breast cancer through the activation of tumor cell-macrophage crosstalk (107). Furthermore, increased expression of COL5A2, a gene encoding a type V collagen alpha chain, has been correlated with poor survival in gastric cancer (109) and colorectal cancer by upregulation of Wnt/β-catenin signaling (108). As a prognostic biomarker, COL5 holds potential for predicting outcomes in pancreatic ductal adenocarcinoma, gastric cancer, laryngeal squamous cell carcinoma, and cervical cancer (110–112).
Type VII collagen (COL7) constitutes a principal component of anchoring fibrils, situated beneath the basal lamina within the dermal-epidermal basement membrane zone of the skin. The diagnostic potential of COL7A1 has also been explored in oral squamous cell carcinoma (OSCC) and oral leukoplakia (OL). Poomsawat et al. conducted a comprehensive study involving 254 samples, revealing that COL7A1 expression was significantly reduced in OSCC compared to normal oral mucosa and OL without dysplasia (113). The research conducted by Oh et al. has demonstrated a significant correlation between COL7A1 expression and the prognosis of patients with gastric cancer. Utilizing DNA microarray analysis, the study compared gene expression profiles between cancerous and non-cancerous gastric tissues. The findings revealed a marked upregulation of COL7A1 in gastric cancer tissues relative to normal tissues. Moreover, patients with intracellular COL7A1 expression exhibited a substantially lower five-year overall survival (OS) rate of 41.5%, in contrast to 69.7% for those with solely extracellular expression. This indicates that the localization of COL7A1 expression serves as an independent prognostic factor, with a hazard ratio of 2.00 (95% CI 1.26-3.16, p=0.003) for OS (114).
Type IX collagen (COL9) is a constituent of the low-abundance collagen family, specifically categorized as FACITs, predominantly localized in cartilage. Its function within the tumor microenvironment remains largely unexamined. To explore the potential of COL9 as a biomarker in oncology, an immunoassay named PRO-C9 was developed, and its technical performance was evaluated for serum analysis. PRO-C9 concentrations were quantified in serum samples from 259 patients diagnosed with various solid tumor types and compared to serum levels from 73 healthy controls. The results indicated that PRO-C9 levels were significantly elevated in patients with solid tumors, including those of the bladder, breast, colorectal, gastric, head and neck, lung, melanoma, ovarian, pancreatic, and renal origins, in comparison to levels observed in healthy controls (115).
Type XII collagen (COL12) has emerged as a potential biomarker for solid tumors due to its elevated levels in the serum of affected patients. A study has developed an ELISA to quantify circulating COL12, underscoring its potential as a non-invasive tool for detecting activated fibroblasts within the tumor microenvironment (103). Moreover, the integrated analysis of mass spectrometry and single-cell transcriptomics reveals that COL12, secreted by CAFs, alters the organization of COL1. This modification contributes to the formation of a pro-invasive microenvironment that promotes metastatic dissemination in breast cancer. Therefore, COL12 has the potential to serve as a biomarker for identifying breast cancer patients who are at an increased risk of metastatic relapse (104).
3 Conclusions and future perspectives
In addition to serving as a structural scaffold for tissues and cells, collagen plays a significant role in various biophysical, biochemical, and cellular alterations that profoundly influence cancer behavior. The precise mechanisms by which collagen operates within tumors remain inadequately understood, with different collagen types exhibiting distinct functions across various tumor types (Table 1). Broadly, the mechanisms of collagen’s action in tumors can be categorized as follows: (1) promotion of tumor growth, invasion, and metastasis; (2) enhancement of extracellular matrix viscosity, which inhibits tumor invasion and metastasis but results in diminished efficacy of chemotherapy and immunotherapy; (3) monitoring of tumor recurrence, serving as a marker for distinguishing between benign and malignant tumors and for prognostication; and (4) targeting in cancer therapy, either through direct collagen degradation or as a target for anti-tumor drugs in vivo (Figure 1).
Figure 1
Figure 1. An examination of the biological role of collagen in tumorigenesis and an overview of contemporary therapeutic approaches.
Table 1
Table 1. Collagens in tumor biology.
Detecting collagen content in primary sites and body fluids using traditional methods is relatively straightforward. However, leveraging collagen detection results to predict tumor recurrence, metastasis, and evaluate treatment efficacy requires further in-depth investigation. This is particularly important given that the type, spatial distribution, and geometric characteristics of collagen significantly influence the biological behavior of tumors. Recent advancements in visualization techniques, such as second-harmonic generation imaging and optical coherence tomography (60, 116, 117), enable detailed characterization of collagen without the need for staining, offering promising potential for clinical application. Furthermore, emerging technologies, including single-cell sequencing, mass spectrometry, and CRISPR-Cas9, have demonstrated significant advantages in the investigation of cancer-associated fibroblasts (CAFs), collagen, and tumor biology. This is particularly evident in pancreatic and breast tumors, which are characterized by a high collagen content (118).
Current collagen-targeted therapies primarily focus on reducing collagen expression and lack strategies to modulate or “normalize” the spatial distribution and geometric characteristics of collagen within the TME. Furthermore, current collagen-targeted therapies may impact non-tumor tissues, potentially resulting in significant side effects. Nevertheless, ongoing advancements and interdisciplinary collaborations in cell biology, oncology, and nanotechnology are likely to facilitate the translation of additional collagen-targeting strategies into clinical applications.
Author contributions
YZ: Conceptualization, Funding acquisition, Writing – original draft. ZJ: Conceptualization, Visualization, Writing – review & editing. LC: Writing – review & editing. JY: Supervision, Writing – review & editing.
Funding
The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. this research was funded by the Special Project of the Science and Technology Plan, Nanchong Science and Technology Bureau(23JCYJPT0061) and the Youth Innovation Project of the Sichuan Medical Association(Q22019).
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Generative AI statement
The author(s) declare that no Generative AI was used in the creation of this manuscript.
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Keywords: collagen, cancer, review, collagen 1, therapeutic target
Citation: Zhou Y, Jiang Z, Cao L and Yang J (2025) The role of various collagen types in tumor biology: a review. Front. Oncol. 15:1549797. doi: 10.3389/fonc.2025.1549797
Received: 22 December 2024; Accepted: 17 February 2025;
Published: 05 March 2025.
Edited by:
Subhradip Karmakar, All India Institute of Medical Sciences, IndiaReviewed by:
Jing Lin, Fourth Medical Center of PLA General Hospital, ChinaKrishna Singh, Johns Hopkins University, United States
Copyright © 2025 Zhou, Jiang, Cao and Yang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Jianquan Yang, bmNzbWNwaGRjeWpxQDE2My5jb20=