未经证实:乙型肝炎病毒(HBV)患者的肝细胞癌(HCC)发病率极高。微小RNA(microRNAs,miRNAs)是一类内源性非编码小RNA,具有新颖的分子治疗机制,在肿瘤的发生发展中起着重要作用。本研究旨在探讨miR-135a和HOXA10在细胞增殖中的调控机制,入侵,和肝癌细胞凋亡。
UNASSIGNED:使用实时定量逆转录聚合酶链反应(qRT-PCR)分析检测miR-135a的表达水平。miR-135a的过表达用于测量miR-135a在增殖中的作用,入侵,和肝癌细胞凋亡。进行双荧光素酶实验以评估HOXA10和miR-135a之间的关系。应用Westernblot观察p-p38、p-ERK、还有p-JNK.
UNASSIGNED:miR-135a在肝癌组织和细胞中的表达水平显著降低。miR-135a过表达抑制肝癌细胞的增殖和侵袭,促进细胞凋亡。重要的是,我们的结果证实HOXA10是miR-135a的直接靶标.在HBV感染下,沉默HOXA10可显著阻断肝癌细胞的增殖和侵袭,促进肝癌细胞凋亡。此外,miR-135a/HOXA10调控p-p38、p-ERK、和p-JNK通过miR-135a/HOXA10轴,从而抑制MAPK途径的激活。
未经证实:HBV促进增殖和侵袭,通过调节miR-135a/HOXA10通路抑制肝癌细胞凋亡。这些发现为提高HBV感染HCC患者的治疗水平提供了理论依据。
UNASSIGNED: The incidence of hepatocellular carcinoma (HCC) in patients with hepatitis B virus (HBV) is extremely high. MicroRNAs (miRNAs) are a type of endogenous non-coding small RNA with novel molecular therapeutic mechanisms that plays an important role in the occurrence and development of cancers. This study aimed to explore the regulation mechanism of miR-135a and
HOXA10 in the proliferation, invasion, and apoptosis of HCC cells.
UNASSIGNED: Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis was used to detect the expression level of miR-135a. Overexpression of miR-135a was used to measure the roles of miR-135a in the proliferation, invasion, and apoptosis of HCC cells. A dual luciferase experiment was performed to assess the relationship between
HOXA10 and miR-135a. Western blot was applied to observe the protein levels of p-p38, p-ERK, and p-JNK.
UNASSIGNED: The expression levels of miR-135a were significantly decreased in HCC tissues and cells. Overexpression of miR-135a inhibited the proliferation and invasion but promoted the apoptosis of HCC cells. Importantly, our results confirmed that
HOXA10 was a direct target of miR-135a. Under HBV infection, silencing of HOXA10 significantly blocked the proliferation and invasion and promoted the apoptosis of HCC cells. In addition, miR-135a/
HOXA10 regulated the expressions of p-p38, p-ERK, and p-JNK through the miR-135a/
HOXA10 axis, thereby inhibiting the activation of the MAPK pathway.
UNASSIGNED: HBV promoted the proliferation and invasion, and inhibited the apoptosis of HCC cells by regulating the miR-135a/HOXA10 pathway. These findings provide a theoretical basis for improving the treatment of HBV-infected HCC patients.