%0 Journal Article
%A Khatun, Ziasmin
%A Saikat, Shoaib
%A Haque, Shaila
%T Src Family Kinases in Epidermal Homeostasis, Wound Healing, and Tumorigenesis
%J Journal of Biosciences and Public Health
%D 2025
%V 1
%N 2
%P 27-40
%R 10.5455/JBPH.2025.08
%U https://www.jbph.org/article/details/src-family-kinases-in-epidermal-homeostasis-wound-healing-and-tumorigenesis
%X The epidermis is primarily composed of keratinocytes, maintain the integrity of skin by carefully controlling the ratio of differentiation to proliferation. Non-receptor tyrosine kinases known as Src family kinases (SFKs), which include Src, Fyn, and Yes, are essential for these processes because they affect tumorigenesis, wound healing, and epidermal maintenance. Through their interactions with receptor tyrosine kinases like EGFR, SFKs modulate keratinocyte migration, differentiation, and proliferation by activating downstream Ras-MAPK and PI3K-Akt pathways. Using integrin-mediated focal adhesion kinase (FAK) activation and cytoskeletal remodeling, SFKs facilitate keratinocyte migration during wound healing. By altering cell adhesion, modifying the epithelial–mesenchymal transition, and abnormally activating proliferative drivers like Yes-associated protein (YAP), dysregulation or overexpression of SFKs disrupts epidermal homeostasis and contributes to carcinogenesis. The development of cutaneous squamous cell carcinoma may be prevented or lessened by targeted inhibition of SFKs, which can be achieved with drugs such as dasatinib, bosutinib, AZD-0530, and bioactive phytochemicals. This review highlights some reported outcomes on the therapeutic approaches targeted at regaining epidermal function, enhancing wound healing, and slowing the spread of cancer while outlining present knowledge of SFK-mediated regulation of keratinocyte biology. Obtaining insight into SFK signaling pathways sets the basis for developing treatments for skin cancers and pathological wound healing.
%K Keratinocyte of epidermis, Proliferation, Src family kinases, Inhibitors, Wound healing, Carcinogenesis, Tumorigenesis
%@ 3104-8749
%I 4Green Research Society
%G English