Lingman Ma
Jiakai Hou
Jian Dong
Yanbo Wang
Jifu Wei- 1School of Life Science and Technology, China Pharmaceutical University, Nanjing, Jiangsu, China
- 2Department of Biology and Biochemistry, University of Houston, Houston, TX, United States
- 3Department of Vascular Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi’an, Shaanxi, China
- 4School of Life Sciences, Nanjing University, Nanjing, China
- 5Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & the Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu, China
Editorial on the Research Topic
How to circumvent the tumour-promoting effect of cytokine in tumour therapy
Cytokines, a class of soluble proteins that are key mediators of cell communication in the tumour microenvironment (TME), can regulate both innate and adaptive immunity (1, 2). Unfortunately, some tumour-related cytokines, especially pro-inflammatory cytokines (such as TNF, IL-6, and IL-1), have a well-recognized tumour-promoting activity and take part in the various phases of tumour initiation and progression (3, 4). Therefore, the research on the tumour-promoting effect of cytokines will play a key role in further revealing the molecular mechanisms of tumour development and identifying novel targets for tumour therapy. In the current Research Topic “How to Circumvent the Tumour-promoting Effect of Cytokine in Tumour Therapy”, we attempted to collect the most-recent progress made in tumour-promoting effect of cytokine. In total, after being peer-reviewed, 5 manuscripts, composed with 3 research articles, 1 review article and 1 brief research report authored by 40 researchers worldwide, were successfully accepted for publication.
Interleukin-32 (IL-32) is an important interleukin cytokine usually linked to innate and adaptive immune responses (5). In recent years, it has been found that IL-32 exhibits both pro- and anti- tumour effects. Aass et al. reported that the activation of toll-like receptors (TLRs) in an inflamed or infectious bone marrow microenvironment may promote IL-32 expression in multiple myeloma cells through NF-κB activation, and this may contribute to accelerating the disease. They therefore propose that the subgroup of IL-32-expressing patients may benefit from combination treatments where antibiotics, antiviral- or anti-inflammatory drugs are included. To evaluate the diagnosis and treatment of tumour patients, the prediction value of cytokine signaling in immune-related genes (CSIRGs) is needed. Pu et al. defined a novel CSIRGs signature in melanoma through applying a machine-learning model by single-cell RNA-sequencing datasets. They discovered a 5-CSIRG signature that was substantially related to the overall survival of melanoma patients, which may assist in predicting melanoma patient prognosis, biological characteristics, and appropriate therapy. Autophagy participated in innate immunity, inflammatory response and adaptive immune response by processing antigens and regulating the development and function of lymphocytes (6–8). Based on R software, Yue et al. found that autophagy score and IFNG expression were novel immunotherapy predictive biomarkers, which might play predictive effects through the JAK-STAT signaling pathway. IFNG might be a potential targeted therapy for cisplatin resistant colon cancer and was also a prognostic indicator. Notably, accumulative evidence suggests that the precancerous stem cells (pCSCs)/CSC niche is an inflammatory dominated milieu where contains different cytokines that function as the key communicators between pCSCs/CSCs and their niche and have a decisive role in promoting cancer development, progression, and metastasis (9, 10). Cui et al. presented a systematic review of current and new insights on cytokines, such as interleukin (IL)-4, IL-6, IL-8, IL-17A, IL-22, IL-23, IL-33 and interferon (IFN)-γ, involving in the modulation of pCSC/CSC properties and features in precancerous and cancerous lesions, and discussed the possible mechanisms of adenoma progression to colorectal cancers (CRCs) and their therapeutic potential. Anaplastic large cell lymphoma (ALCL) is characterized by the presence of large anaplastic cells with diffuse and strong expression of CD30 on the cell membrane and in the Golgi region (11). Xiang et al. reported that pSTAT3-Y705/S727 can be used to help distinguish ALK-negative ALCL from CD30high PTCL, NOS, and pSTAT3-S727 expression by tumour infiltrating lymphocytes could predict the prognosis of a subset of PTCL, NOS.
In conclusion, increasing evidence shows that cytokines are heavily involved in regulating both pro- and anti- tumour activities, such as immune activation and suppression, inflammation, cell damage, angiogenesis, cancer stem-cell-like cell maintenance, invasion, metastasis and etc. New insights into the prognosis and treatment of tumour patients may be provided by the in-depth study of tumour-related cytokines.
Author contributions
LM: Conceptualization, Writing – original draft, Writing – review & editing. JH: Conceptualization, Writing – original draft. JD: Conceptualization, Writing – original draft. YW: Conceptualization, Writing – original draft. JW: Conceptualization, Writing – original draft.
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.
Publisher’s note
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References
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Keywords: tumour-promoting effect, cytokine, tumour therapy, interleukin-32, cytokine signaling in immune-related genes
Citation: Ma L, Hou J, Dong J, Wang Y and Wei J (2023) Editorial: How to circumvent the tumour-promoting effect of cytokine in tumour therapy. Front. Immunol. 14:1298157. doi: 10.3389/fimmu.2023.1298157
Received: 21 September 2023; Accepted: 03 October 2023;
Published: 10 October 2023.
Edited and Reviewed by:
Cinzia Fionda, Sapienza University of Rome, ItalyCopyright © 2023 Ma, Hou, Dong, Wang and Wei. 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: Lingman Ma, bWFsaW5nbWFuMTk4N0AxMjYuY29t