Collectively, our results demonstrated that miR-6734 inhibits the growth of colon cancer cells by up-regulating p21 gene expression and subsequent induction of cell cycle arrest and apoptosis, suggesting its role as an important endogenous regulator of cancer cell proliferation and survival.
The cyclin-dependent kinase (CDK) inhibitor 1A, p21/Cip1, is a vital cell cycle regulator, dysregulation of which has been associated with a large number of human malignancies.
Involvement of the DNA damage response and p21(CIP1) defines a novel mechanism of RD action and indicates that RD could be further developed as a promising anticancer agent for cancer therapy.
Here, we show that loss of the p53 target gene cyclin-dependent kinase inhibitor 1A (CDKN1A, also known as p21(WAF1/CIP1)) increases apoptosis induction following telomerase inhibition in a variety of cancer cell lines and mouse xenografts.
Ionizing radiation and chemotherapy activate AMPK in cancer cells to mediate signal transduction downstream of ataxia telangiectasia mutated (ATM) to activate p53- p21(cip1)/p27(kip1) and inhibit mTOR.
We further demonstrate the correlation of apoptotic sensitivity to zinc and Smad4 and PIAS1 in multiple cancer cell lines, demonstrating that the important roles of PIAS1, Smad2, and Smad4 in zinc-induced cell death and p21(WAF1/Cip1) transactivation were common biological events in different cancer cell lines.
p21(WAF(1)/)(CIP(1)) is a well-known cell cycle regulatory protein which is overexpressed in several cancer cell lines, and known to determine cell fate.
Global inhibition of class I and II histone deacetylases (HDACs) stops cancer cell proliferation in vitro and has proven effective against cancer in clinical trials, at least in part, through transcriptional reactivation of the p21(WAF1/Cip1)gene.
It has been reported that CCND1, p21(cip1)DCC, MTHFR, and EXO1 are related with the risk of malignant neoplasm, but few studies have mentioned the prognosis of the patients.
Curcumin inhibits cancer cell proliferation in part by suppressing cyclin D1 and inducing expression of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1).
The tumor suppressor gene p53 and its downstream effector p21(CDKN1A/WAF1/CIP1) are thought to play major roles in the development of human malignancy.
In this study, we have attempted to address the question of whether RUNX1/AML1, acting both as a gene transcription activator and a repressor, depending on the context, can be correlated with the expression of p21WAF1/CIP1 in gynecologic malignancies, in particular in EEC, where the role of p21(WAF1/CIP1) remains controversial.
Although there are many controversial reports about the effect of p53 and p21(WAF1/CIP1) overexpression in different human tumor cells, the p53 gene is shown to be a more effective candidate for cancer gene therapy because of its more pronounced ability to induce apoptosis.
We conclude that antisense imaging of upregulated p21(WAF-1/CIP-1) gene expression is feasible and could represent a promising new molecular imaging strategy for monitoring tumor response in cancer patients.
We have found that the cyclin-dependent kinase inhibitor p21(WAF1/cip1) plays a major role in regulating several aspects of mucosal homeostasis and the response to dietary and pharmacologic modulators of tumorigenesis; that disruption of lineages of differentiation of intestinal epithelial cells are intimately involved in tumor formation; and that important pathways that contribute to normal homeostasis and cancer development may be coordinately regulated by mitochondrial function, with the mitochondrial membrane potential playing a key role.