Tumor Protein p63/microRNA Network in Epithelial Cancer Cells
Edward A. Ratovitski
Affiliation: Department of Otolaryngology/ Head and Neck Surgery, Head and Neck Cancer Research Division, The Johns Hopkins University School of Medicine, Cancer Research Building II, 1550 Orleans Street, Baltimore, MD 21231, U.S.A.
Keywords: Apoptosis, Autophagy, Cell cycle arrest, Cell metabolism, Chemoresistance, Epigenetics, microRNA, TP63.
Non-coding microRNAs are involved in multiple regulatory mechanisms underlying response of cancer cells to
stress leading to apoptosis, cell cycle arrest and autophagy. Many molecular layers are implicated in such cellular response
including epigenetic regulation of transcription, RNA processing, metabolism, signaling. The molecular interrelationship
between tumor protein (TP)-p53 family members and specific microRNAs is a key functional network supporting
tumor cell response to chemotherapy and potentially playing a decisive role in chemoresistance of human epithelial cancers.
TP63 was shown to modulate the expression of numerous microRNAs involved in regulation of epithelial cell proliferation,
differentiation, senescence, “stemness” and skin maintenance, epithelial/ mesenchymal transition, and tumorigenesis
in several types of epithelial cancers (e.g. squamous cell carcinoma, ovarian carcinoma, prostate carcinoma, gastric
cancer, bladder cancer, and breast tumors), as well as in chemoresistance of cancer cells. TP63/microRNA network
was shown to be involved in cell cycle arrest, apoptosis, autophagy, metabolism and epigenetic transcriptional regulation,
thereby providing the groundwork for novel chemotherapeutic venues.
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