Tumor-suppressor genes, cell cycle regulatory checkpoints, and the skin

Abstract

The cell cycle (or cell-division cycle) is a series of events that take place in a cell, leading to its division and duplication. Cell division requires cell cycle checkpoints (CPs) that are used by the cell to both monitor and regulate the progress of the cell cycle. Tumor-suppressor genes (TSGs) or antioncogenes are genes that protect the cell from a single event or multiple events leading to cancer. When these genes mutate, the cell can progress to a cancerous state. We aimed to perform a narrative review, based on evaluation of the manuscripts published in MEDLINE-indexed journals using the Medical Subject Headings (MeSH) terms “tumor suppressor's genes,” “skin,” and “cell cycle regulatory checkpoints.” We aimed to review the current concepts regarding TSGs, CPs, and their association with selected cutaneous diseases. It is important to take into account that in some cell cycle disorders, multiple genetic abnormalities may occur simultaneously. These abnormalities may include intrachromosomal insertions, unbalanced division products, recombinations, reciprocal deletions, and/or duplication of the inserted segments or genes; thus, these presentations usually involve several genes. Due to their complexity, these disorders require specialized expertise for proper diagnosis, counseling, personal and family support, and genetic studies. Alterations in the TSGs or CP regulators may occur in many benign skin proliferative disorders, neoplastic processes, and genodermatoses.

OVCA1 expression and its correlation with the expression levels of cyclin D1 and p16 in cervical cancer and intraepithelial neoplasia

“…Through the competitive inhibition of cyclin D1, p16 protein is able to function directly in the process of cell cycle regulation to reduce cell proliferation (42–44). Furthermore, p16 expression levels are negatively regulated by pRb protein (45).…”

Skin manifestations associated with kidney cancer

“…Von Hippel-Lindau (VHL) disease is an uncommon, autosomal dominant familial cancer syndrome that results from inactivation of the tumor suppressor VHL gene, which serves to inhibit expression of pro-angiogenic hypoxia-inducible genes [23]. Affected individuals have increased risk of developing highly vascular tumors, including clear cell RCCs, central nervous system hemangioblastomas, retinal angiomas, and pheochromocytomas, which often present by the fourth decade in life [24].…”

Emodin Downregulates Cell Proliferation Markers During Dmba Induced Oral Carcinogenesis in Golden Syrian Hamsters

“…Cell-cycle disruption is the major characteristic features of neoplastic transformation and the status of cell-cycle regulators can thus be utilized to assess the prognostic significance in patients with cancer. Disturbance in the cell-cycle regulation is the hallmark of carcinogenesis (Velez et al, 2015;Bertoli et al, 2013).…”