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通过靶向……抑制乙肝病毒感染的肝癌细胞的增殖。 (原句不完整,缺少具体靶向内容)

inhibits the proliferation of HBV-infected hepatocellular carcinoma cells by targeting .

作者信息

Lin Jianjun, Lian Xiang, Xue Shihang, Ouyang Lian, Zhou Lihui, Lu Yuyang, Xie Longteng

机构信息

Clinical Laboratory Department, Xiangshan First People's Hospital, Ningbo Fourth Hospital, Ningbo, China.

Hepatology Department, Xiangshan First People's Hospital, Ningbo Fourth Hospital, Ningbo, China.

出版信息

Transl Cancer Res. 2023 Jan 30;12(1):135-149. doi: 10.21037/tcr-22-2789. Epub 2023 Jan 16.

DOI:10.21037/tcr-22-2789
PMID:36760373
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9906062/
Abstract

BACKGROUND

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 and in the proliferation, invasion, and apoptosis of HCC cells.

METHODS

Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis was used to detect the expression level of . Overexpression of was used to measure the roles of in the proliferation, invasion, and apoptosis of HCC cells. A dual luciferase experiment was performed to assess the relationship between and . Western blot was applied to observe the protein levels of , , and .

RESULTS

The expression levels of were significantly decreased in HCC tissues and cells. Overexpression of inhibited the proliferation and invasion but promoted the apoptosis of HCC cells. Importantly, our results confirmed that was a direct target of . Under HBV infection, silencing of significantly blocked the proliferation and invasion and promoted the apoptosis of HCC cells. In addition, / regulated the expressions of p-p38, p-ERK, and p-JNK through the / axis, thereby inhibiting the activation of the MAPK pathway.

CONCLUSIONS

HBV promoted the proliferation and invasion, and inhibited the apoptosis of HCC cells by regulating the / pathway. These findings provide a theoretical basis for improving the treatment of HBV-infected HCC patients.

摘要

背景

乙型肝炎病毒(HBV)感染患者中肝细胞癌(HCC)的发病率极高。微小RNA(miRNAs)是一类具有新型分子治疗机制的内源性非编码小RNA,在癌症的发生和发展中起重要作用。本研究旨在探讨[具体miRNA名称1]和[具体miRNA名称2]对HCC细胞增殖、侵袭和凋亡的调控机制。

方法

采用实时定量逆转录聚合酶链反应(qRT-PCR)分析检测[具体miRNA名称1]的表达水平。通过过表达[具体miRNA名称1]来检测其对HCC细胞增殖、侵袭和凋亡的作用。进行双荧光素酶实验以评估[具体miRNA名称1]和[具体miRNA名称2]之间的关系。应用蛋白质免疫印迹法观察[相关蛋白名称1]、[相关蛋白名称2]和[相关蛋白名称3]的蛋白水平。

结果

HCC组织和细胞中[具体miRNA名称1]的表达水平显著降低。过表达[具体miRNA名称1]可抑制HCC细胞的增殖和侵袭,但促进其凋亡。重要的是,我们的结果证实[具体miRNA名称2]是[具体miRNA名称1]的直接靶点。在HBV感染下,沉默[具体miRNA名称2]可显著阻断HCC细胞的增殖和侵袭,并促进其凋亡。此外,[具体miRNA名称1]/[具体miRNA名称2]通过[具体miRNA名称1]/[具体miRNA名称2]轴调节p-p38、p-ERK和p-JNK的表达,从而抑制MAPK通路的激活。

结论

HBV通过调节[具体miRNA名称1]/[具体miRNA名称2]通路促进HCC细胞的增殖和侵袭,并抑制其凋亡。这些发现为改善HBV感染的HCC患者的治疗提供了理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/31abbf57d6a9/tcr-12-01-135-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/ba4bf23610e1/tcr-12-01-135-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/f63de5e65632/tcr-12-01-135-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/6196c6932a6b/tcr-12-01-135-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/b8ea4f5b0b01/tcr-12-01-135-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/588068f4f0cb/tcr-12-01-135-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/7c030b485234/tcr-12-01-135-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/7d334d72af43/tcr-12-01-135-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/2338211d90b0/tcr-12-01-135-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/31abbf57d6a9/tcr-12-01-135-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/ba4bf23610e1/tcr-12-01-135-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/f63de5e65632/tcr-12-01-135-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/6196c6932a6b/tcr-12-01-135-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/b8ea4f5b0b01/tcr-12-01-135-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/588068f4f0cb/tcr-12-01-135-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/7c030b485234/tcr-12-01-135-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/7d334d72af43/tcr-12-01-135-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/2338211d90b0/tcr-12-01-135-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96d6/9906062/31abbf57d6a9/tcr-12-01-135-f9.jpg

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