当前位置: X-MOL 学术Cancer Sci. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Hepatitis B virus-regulated growth of liver cancer cells occurs through the microRNA-340-5p-activating transcription factor 7-heat shock protein A member 1B axis.
Cancer Science ( IF 5.7 ) Pub Date : 2019-04-11 , DOI: 10.1111/cas.14004
Feifei Song 1 , Mingcong Wei 1 , Jingwen Wang 1 , Yang Liu 1 , Mingxiong Guo 2 , Xiaolu Li 3 , Jun Luo 4 , Junying Zhou 4 , Min Wang 1 , Deyin Guo 5 , Lang Chen 1 , Guihong Sun 1, 6
Affiliation  

Hepatocellular carcinoma (HCC) is a common cancer with poor prognosis. Hepatitis B virus (HBV) is one of the leading causes of HCC, but the precise mechanisms by which this infection promotes cancer development are not fully understood. Recently, miR-340-5p, a microRNA (miRNA) that has been identified as a cancer suppressor gene, was found to inhibit the migration and invasion of liver cancer cells. However, the effect of miR-340-5p on cell proliferation and apoptosis in HBV-associated HCC remains unknown. In our study, we show that miR-340-5p plays an important role during HBV infection and hepatocellular carcinoma development. Specifically, this miRNA directly binds to the mRNA encoding activating transcription factor 7 (ATF7), a protein that both promotes cell proliferation and suppresses apoptosis through its interaction with heat shock protein A member 1B (HSPA1B). We further found that miR-340-5p is downregulated by HBV, which enhances ATF7 expression, leading to enhanced cell proliferation and inhibition of apoptosis. Notably, ATF7 is upregulated in HCC tissue, suggesting that HBV may target miR-340-5p in vivo to promote ATF7/HSPA1B-mediated proliferation and apoptosis and regulate liver cancer progression. This work helps to elucidate the complex interactions between HBV and host miRNAs and further suggests that miR-340-5p may represent a promising candidate for the development of improved therapeutic strategies for HCC.

中文翻译:

乙肝病毒调节的肝癌细胞生长是通过microRNA-340-5p激活转录因子7-热休克蛋白A的1B轴发生的。

肝细胞癌(HCC)是预后较差的常见癌症。乙型肝炎病毒(HBV)是HCC的主要原因之一,但这种感染促进癌症发展的确切机制尚不完全清楚。最近,发现miR-340-5p(一种已被鉴定为癌症抑制基因的miRNA)可以抑制肝癌细胞的迁移和侵袭。但是,miR-340-5p对与HBV相关的HCC细胞增殖和凋亡的影响仍然未知。在我们的研究中,我们表明miR-340-5p在HBV感染和肝细胞癌的发展中起着重要作用。具体来说,该miRNA直接与编码激活转录因子7(ATF7)的mRNA结合,通过与热休克蛋白A成员1B(HSPA1B)相互作用,既促进细胞增殖又抑制凋亡的蛋白质。我们进一步发现miR-340-5p被HBV下调,从而增强ATF7表达,从而导致细胞增殖增强和凋亡抑制。值得注意的是,ATF7在HCC组织中上调,表明HBV可能在体内靶向miR-340-5p,以促进ATF7 / HSPA1B介导的增殖和凋亡并调节肝癌的进展。这项工作有助于阐明HBV与宿主miRNA之间的复杂相互作用,并进一步表明,miR-340-5p可能代表了开发改进的HCC治疗策略的有希望的候选者。导致细胞增殖增强和凋亡抑制。值得注意的是,ATF7在HCC组织中上调,表明HBV可能在体内靶向miR-340-5p,以促进ATF7 / HSPA1B介导的增殖和凋亡并调节肝癌的进展。这项工作有助于阐明HBV与宿主miRNA之间的复杂相互作用,并进一步表明,miR-340-5p可能代表了开发改进的HCC治疗策略的有希望的候选者。导致细胞增殖增强和凋亡抑制。值得注意的是,ATF7在HCC组织中上调,表明HBV可能在体内靶向miR-340-5p,以促进ATF7 / HSPA1B介导的增殖和凋亡并调节肝癌的进展。这项工作有助于阐明HBV与宿主miRNA之间的复杂相互作用,并进一步表明,miR-340-5p可能代表了开发改进的HCC治疗策略的有希望的候选者。
更新日期:2019-11-01
down
wechat
bug