Rabbit Anti-Human PRKCD Polyclonal antibody

The purpose of this study was to define the roles of miR-181a in determining sensitivity of cervical cancer to radiation therapy, to explore the underlying mechanism and to evaluate the potential of miR-181a as a biomarker for predicting radio-sensitivity. Tumor specimens from 18 patients with a histological diagnosis of squamous cervical carcinoma (stage IIIB) were used in the micro-RNA profiling and comparison. These patients never received any chemotherapy before radiation therapy. Human cervical cancer cell lines, SiHa and Me180, were used in vitro (cell culture) and in vivo (animal) studies. Transfection of tumor cells with the mimic or inhibitor of miR-181a, and reporter gene assay, were performed to investigate the role of miR-181a in determining radio-sensitivity and the target gene. Higher expression of miR-181a was observed in human cervical cancer specimens and cell lines that were insensitive to radiation therapy, as compared with sensitive cancer specimens and the cell lines. We also found that miR-181a negatively regulated the expression of PRKCD, a pro-apoptotic protein kinase, via targeting its 3'-untranslated region (UTR), thereby inhibiting irradiation-induced apoptosis and decreasing G(2)/M block. The role of miR-181a in conferring cellular resistance to radiation treatment was validated both in cell culture models and in mouse tumor xenograft models. The effect of miR-181a on radio-resistance was mediated through targeting the 3'-UTR of PRKCD gene. Thus, the expression level of miR-181a in cervical cancer may serve as a biomarker for sensitivity to radiation therapy, and targeting miR-181a may represent a new approach to sensitizing cervical cancer to radiation treatment.

As a widespread environmental contaminant, bisphenol A (2,2-bis(4-hydroxyphenyl)propane, BPA) has been implicated in male reproductive function injury. Previous studies have investigated the mechanisms of DNA damage and oxidative stress caused by BPA; however, little is known regarding its impact on DNA methylation. In this paper, we assessed the adverse effects of BPA on mouse spermatocytes and investigated a potential role of DNA methylation. We demonstrated that BPA exposure inhibited cell proliferation, reduced the DNA replication capacity, and triggered apoptosis in GC-2 cells. In addition, the global DNA methylation levels increased, and the relative expression levels of DNA methyltransferases (DNMTs) varied following BPA exposure. Thousands of distinct methylated sites were screened using microarray analysis. The expressions of myosin-binding protein H (mybph) and protein kinase C delta (prkcd) were verified to be regulated by DNA methylation. These findings indicate that BPA had toxicity in spermatocytes, and DNA methylation may play a vital role in the regulation of BPA-triggered spermatocyte toxicity. (C) 2016 Elsevier B.V. All rights reserved.