Hair Follicle Stem Cell and its Niche in Normal vs Cancerous Development

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About this Research Topic

Submission deadlines

  1. Manuscript Submission Deadline 22 March 2025

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Background

Hair follicles (HF) regenerate throughout adult life, involving a 2-way signaling between epithelial stem cells and its niche. The niche includes mesenchymal cells such as dermal papillae and fibroblasts, immune cells, endothelial cells, melanocytes, and adipocytes to name a few. HF induction by dermal papillae involves a plethora of signaling molecules such as Wnt and Bmp crosstalk together with Fgf, Shh, Igf. Tgfb and other metabolic pathways. Misexpression of some of these factors cause abnormal receptor-ligand interaction leading to abnormal hair cycling or could potentially result in tumorigenic outcome with a specific "cell of origin" for cancer. Basal Cell Carcinoma (BCC) is a vivid example of malignancy derived from hair follicle or touch dome stem cells due to uncontrolled hedgehog signaling. While Ras mutations are shown to be integrated and contained by HFSCs, the non-cycling upper epidermis is driven towards oncogenic outgrowth. Keratoacanthomas is a disease of abnormal hair follicle regression suggesting a HFSC disease. On the other hand, Fgfr2b epidermal KO mice show signs of dysplasia and develops spontaneous papilloma suggesting a tumor protective role of Fgf signaling in skin. Another common type of skin cancer, melanoma, can be driven by various signaling changes, including abnormal MAPK signaling, uncontrolled cell cycle progression, alterations in the AKT pathway, and other less common mutations for sporadic cases. Hair follicle compartmentalization often provides "physical or immunologic barrier" to the spread of tumor cells deep down in the skin implying dermal-epidermal junctions as an important signaling checkpoint. Immune cells and adipocytes enable the mechanical and nutritional sensing of the tissue architecture while nerves/vasculature help transmit the signal to facilitate niche response. Understanding the epithelial stem cells and their niche interactions in the context of normal vs cancerous stem cell renewal and maintenance thus remains an interesting research question to explore.

The goal of this research topic is to enhance the understanding of the complex interactions between stem cells and their niches in pathological condition such as cancers, with a focus on skin stem cells e.g., HFSC and epidermal stem cells.
Stem cells of the skin are essential and are continuously replenished during hair cycle, hair loss and skin regeneration, ageing and repair. However, malfunctions in stem cell machinery and balance can be deleterious and lead to tumor initiation, triggered by replication error or external stimuli such as ultraviolet (UV) radiation. For instance, squamous cell carcinoma results from UV-induced clonal expansion of epidermal cells, while excess melanocyte proliferation leads to malignant melanoma.Intrinsic factors like stem cell plasticity are crucial for tissue survival under injury, inflammation, genetic predisposition, or other pathological conditions. Yet, this plasticity can also turn into an unwanted tumorigenic force, as seen in intestinal tumor resulting from YAP/TAZ activation. The ability of stem cells to de-differentiate and revert to a stem cell state under adverse conditions can also initiate tumors.

In this issue, we expect authors to explore stem cell-niche interactions within the cancer microenvironment. We are particularly interested in studies utilizing mouse models of tumors that exhibit progressive hair phenotypes followed by oncogenic invasion, highlighting the role of various altered signaling molecules. We aim to focus on how the niche reprograms itself to either combat or facilitate cancer initiation. Depending on the tumor type and the “cell-of-origin,” authors should examine how niche responses differ and how they are influenced by aging or other pathological conditions. Additionally, we seek insights into whether disrupting cancer-specific niche responses can restore normal stem cell growth. Contributors should aim to delineate the specific signaling switches that drive stem cells from normal to cancerous states and propose interventions to revive normal niche interactions.

We invite researchers to submit original research articles, reviews, and perspectives that address the following themes:
• Mechanisms of stem cell-niche interactions in the cancer microenvironment
• The role of niche reprogramming in either resisting or promoting cancer initiation
• Differences in niche responses based on tumor type and cell-of-origin
• Impact of aging and other pathological conditions on niche responses
• Strategies to disrupt cancer-specific niche interactions and restore normal stem cell growth
• Identification of signaling pathways and molecular switches involved in the transition from normal to cancerous states

By contributing to this Research Topic, authors will help advance our understanding of stem cell biology and cancer, potentially leading to new therapeutic strategies for enhancing tissue repair and preventing tumorigenesis.

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This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

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Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

  • Brief Research Report
  • Data Report
  • Editorial
  • General Commentary
  • Hypothesis and Theory
  • Methods
  • Mini Review
  • Opinion
  • Original Research
  • Perspective
  • Review
  • Technology and Code

Keywords: HFSC, Niche, Mesenchyme, DP, Fibroblasts, immune cells, squamous cell carcinoma

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