The Emerging Role of p27 in Development of Diseases.
The cell cycle regulation and tumor suppressor p27 encoded by CDKN1B plays a key role in many cellular events. p27 is a member of the Cip/Kip family of cyclin-dependent kinase inhibitors, which functions to negatively regulate cell cycle progression at the G1/S boundary in response to antiproliferative stimuli.
In addition, numerous p27 functions, not related to CDK inhibition, have been described. For instance, cytosolic p27 plays a role in the regulation of cytoskeleton assembly/disassembly, therefore, regulates the cell morphology and movement.
In addition, p27 is involved in apoptosis and autophagy modulation. Mutations, expression and mislocalization of p27 have been found in many diseases suggesting the important role of p27 in the pathogenesis of diseases. Human p27 gene was cloned in 19947 and mapped to chromosome 12p13.
Later on, p27 mutations were discovered in several types of human cancers including breast cancer
sporadic parathyroid adenomas, endocrine neoplasia, small intestine neuroendocrine tumors. Several types of tumors show decreased expression of p27, including breast, colon, esophageal carcinomas, head and
neck cancers, hematological tumors lung, prostate, melanomas and ovarian tumors. The decreased expression of p27 is due to increased proteasome-mediated protein degradation, correlates with poor prognosis of patients. Several other studies demonstrate that a decrease in the expression levels of p27 protein contributes to tumor development by increasing in CDK activity and cell proliferation. In addition, an increased body of evidence demonstrates that mislocalization of p27 contributes to the development of aggressive phenotype and anticancer therapy resistance.
Cancer Stud Mol Med Open J. 2018; 4(1): e1-e2. doi: 10.17140/CSMMOJ-4-e006