HBx promotes cell proliferation by disturbing the cross-talk between miR-181a and PTEN

Tian, Yi; Xiao, Xuewen; Gong, Xing; Peng, Feng; Yun, Xu; Jiang, Yongfang; Gong, Guozhong

doi:10.1038/srep40089

Cited by 27 publications

(19 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, the level of miR-181a in HCC tissues was significantly higher than that in the normal liver tissues. Hepatitis B virus (HBV) is involved in the initiation and progression of HCC, the expression of miR-181a was strongly up-regulated in HBV-expressing cells or HCC cells [29, 31, 32]. Liu et al used miRNA microarrays and northern blotting analyses to compare the expression profile of cellular miRNAs of a stable HBV-expressing cell line (HepG2.2.15) and its parent cell line HepG2, and the results showed that the expression of miR-181a, miR-181b, miR-200b, and miR-146a were all up-regulated in HepG2.2.15 cells [33].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA XIST regulates PTEN expression by sponging miR-181a and promotes hepatocellular carcinoma progression

et al. 2017

View full text Add to dashboard Cite

BackgroundTumor metastasis often occurs in hepatocellular carcinoma (HCC) and influences the patient’s prognosis, and microRNAs are reported to play key roles in tumor metastasis. This study was conducted to explore the effect of microRNAs on HCC metastasis.MethodsThe levels of miR-181a in HCC tissues, adjacent tissues, metastatic HCC tissues, and non-metastatic HCC tissues at different stages were determined by qRT-PCR. Effect of miR-181a on the proliferation, invasion, and metastasis of HCC cells was estimated by cell counting kits-8 (CCK-8), wound-healing, and Transwell assays. Software analysis and luciferase assays were used to explore the target gene of miR-181a.ResultsMiR-181a was up-regulated in HCC tissues and its expression level in metastatic HCC tissues was much higher than in non-metastasis samples. PTEN was found to be a target gene of miR-181a. MiR-181a had multiple binding sites with the long non-coding RNA (lncRNA) XIST. The regulation of miR-181a on PTEN was mediated by lncRNA XIST. The proliferation and invasion of cells with siXIST were significantly enhanced compared with those of control cells, while knockdown of miR-181a abolished the enhancing effects.ConclusionsMiR-181a can promote HCC metastasis by targeting PTEN, which is regulated by lncRNA XIST.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-017-3216-6) contains supplementary material, which is available to authorized users.

show abstract

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA XIST regulates PTEN expression by sponging miR-181a and promotes hepatocellular carcinoma progression

et al. 2017

View full text Add to dashboard Cite

show abstract

“…HBx, a key regulatory HBV protein that is important for HBV replication, is involved in the initiation and progression of HCC (20). Research has demonstrated that HBx leads to cell proliferation and is involved in the initiation of HCC (20,21). A previous study confirmed the colocalization of HBx with COXIII and the upregulation of ROS generation in HL7702 and HepG2 cells, and ROS from mitochondria induced COX-2 expression that promoted HepG2 cell growth (5,6).…”

Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

HBx promotes the proliferative ability of HL‑7702 cells via the COX‑2/Wnt/β‑catenin pathway

et al. 2018

View full text Add to dashboard Cite

Hepatitis B virus X protein (HBx) has been termed a viral oncoprotein, and is involved in the initiation and progression of hepatocellular carcinoma (HCC). Cyclooxygenase‑2 (COX‑2) and β‑catenin have been attributed to the oncogenic activity of HBx in HBV‑associated HCC. The present study aimed to determine whether there is crosstalk between COX‑2 and the Wnt/β‑catenin signaling pathway during HL‑7702‑HBx cell proliferation, and to investigate the associated underlying molecular mechanism. In the present study, cell proliferation assay, colony formation assay and flow cytometric analysis were used to detect the proliferative ability of cells. Reverse transcription‑quantitative polymerase chain reaction and western blotting were performed to examine the mRNA and protein expression of COX‑2, β‑catenin, cyclin‑D1 and c‑myc. The results demonstrated that HL‑7702‑HBx exhibited increased cell proliferation, higher colony formation efficiency and a shortened G1 period of the cell cycle. In addition, the mRNA and protein expression levels of COX‑2 were increased, and this was associated with HL‑7702‑HBx cell growth. Furthermore, the expression of β‑catenin and its target genes, cyclin‑D1 and c‑myc proto‑oncogene protein, was upregulated by HBx via COX‑2. Finally, HBx promoted HL‑7702 cell proliferation through the Wnt/β‑catenin signaling pathway. In conclusion, the primary finding of the present study was that HBx may promote HL‑7702 cell proliferation via the COX‑2/Wnt/β‑catenin pathway. Thus, it may be helpful to further investigate the molecular mechanism of HBV‑associated hepatocellular carcinoma.

show abstract

“…PTEN inhibits PI3K-Akt and protects p53 by attenuating the mouse double minute 2 homolog (Mdm2) translocation into the nucleus ( Figure 1 ) [ 134 ]. Upregulation of miR-181a suppresses PTEN expression, and inhibition of miR-181a abolishes the inhibitory effect of HBX on PTEN protein [ 135 ]. A novel lncRNA DBH-AS1 has been shown to activate ERK/p38/JNK MAPK (extracellular signal-regulated kinases/p38/ c-Jun N-terminal kinases mitogen-activated protein kinase) signaling and promote cell proliferation.…”

Section: Hepatitis B Virus and Apoptosismentioning

confidence: 99%

Interference of Apoptosis by Hepatitis B Virus

Lin

Zhang

2017

Viruses

View full text Add to dashboard Cite

Hepatitis B virus (HBV) causes liver diseases that have been a consistent problem for human health, leading to more than one million deaths every year worldwide. A large proportion of hepatocellular carcinoma (HCC) cases across the world are closely associated with chronic HBV infection. Apoptosis is a programmed cell death and is frequently altered in cancer development. HBV infection interferes with the apoptosis signaling to promote HCC progression and viral proliferation. The HBV-mediated alteration of apoptosis is achieved via interference with cellular signaling pathways and regulation of epigenetics. HBV X protein (HBX) plays a major role in the interference of apoptosis. There are conflicting reports on the HBV interference of apoptosis with the majority showing inhibition of and the rest reporting induction of apoptosis. In this review, we described recent studies on the mechanisms of the HBV interference with the apoptosis signaling during the virus infection and provided perspective.

show abstract

HBx promotes cell proliferation by disturbing the cross-talk between miR-181a and PTEN

Cited by 27 publications

References 30 publications

Long non-coding RNA XIST regulates PTEN expression by sponging miR-181a and promotes hepatocellular carcinoma progression

Long non-coding RNA XIST regulates PTEN expression by sponging miR-181a and promotes hepatocellular carcinoma progression

HBx promotes the proliferative ability of HL‑7702 cells via the COX‑2/Wnt/β‑catenin pathway

Interference of Apoptosis by Hepatitis B Virus

Contact Info

Product

Resources

About