Long non-coding RNA XIST promotes cell growth by regulating miR-139-5p/PDK1/AKT axis in hepatocellular carcinoma

Mo, Yichao; Lu, Yaoyong; Wang, Peng; Huang, Shiyun; He, Longguang; Li, Dasheng; Li, Fuliang; Huang, Jun; Lin, Xiaoxia; Li, Xueru; Che, Siyao; Chen, Qinshou

doi:10.1177/1010428317690999

Cited by 76 publications

(64 citation statements)

References 27 publications

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“…LncRNA XIST is important to silence one X‐chromosome during female development. Many studies have reported that abnormal XIST expression can lead to human cancers . For instance, XIST was responsible for hepatocellular carcinoma development through regulating miR‐139‐5p/PDK1 axis .…”

Section: Introductionmentioning

confidence: 99%

XIST promotes gastric cancer (GC) progression through TGF‐β1 via targeting miR‐185

Zhang

Chen²,

Liu

et al. 2017

J of Cellular Biochemistry

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LncRNAs and microRNAs can play significant roles in various cancers, including gastric cancer (GC). In our study, we investigated the role of lncRNA XIST in GC. We observed that XIST was increased in MGC803 and BGC823 cells compared to human normal gastric epithelial GES-1 cells. It was also shown that miR-185 was decreased in GC cell lines. Silencing XIST can inhibit the growth of GC cells and bioinformatics analysis was performed to confirm the correlation between XIST and miR-185. Interestingly, a negative correlation was indicated between XIST and miR-185 in GC cells. In addition, TGF-β1 was predicted as a target gene of miR-185. miR-185 can modulate TGF-β1 expression negatively in vitro. Moreover, we found that sh-XIST inhibited GC development via decreasing TGF-β1 by upregulating miR-185 in vitro. Therefore, we speculated that XIST can act as a competing endogenous lncRNA (ceRNA) to regulate TGF-β1 by sponging miR-185 in GC. Taken these together, it was indicated that XIST/miR-185/TGF-β1 axis participated in the development of GC. XIST could act as a potential prognostic biomarker in GC development.

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Section: Introductionmentioning

confidence: 99%

XIST promotes gastric cancer (GC) progression through TGF‐β1 via targeting miR‐185

Zhang

Chen²,

Liu

et al. 2017

J of Cellular Biochemistry

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“…Moreover, functional studies have indicated that some lncRNAs are involved in cancer pathogenesis and progression in humans, acting as oncogenes or tumor suppressors. For instance, Mo et al reported that the lncRNA XIST is up-regulated in HCC tissues and cell lines and can promote cell growth in this cancer [23], and Yuan et al established that HCC cell stemness features are increased by DANCR, another lncRNA, via derepression of CTNNB1 [24]. However, the functional and clinical significance of many lncRNAs and the molecular mechanisms responsible remain incompletely understood.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA CASC2c inhibited cell proliferation in hepatocellular carcinoma by inactivated ERK1/2 and Wnt/β-catenin signaling pathway

Yang

Liu

et al. 2019

Clin Transl Oncol

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Purpose Long non-coding RNAs (lncRNAs) have been shown to play important roles in tumorigenesis, but their biological functions and the underlying molecular mechanisms remain unclear. Alternative splicing of five exons results in three transcript variants of cancer susceptibility 2 (CASC2): the lncRNAs CASC2a, CASC2b, and CASC2c. CASC2a/b have been found to have crucial regulatory functions in a number of malignancies, but few studies have examined the effects of CASC2c in cancers. The objective of the study was to investigate the role of CASC2c in the proliferation and apoptosis of hepatocellular carcinoma (HCC) cells. Methods This study first investigated the expression levels of CASC2c in tumor tissues, corresponding non-tumor tissues and cells using quantitative real-time polymerase chain reaction. The function and underlying molecular mechanism of CASC2c in human HCC were investigated in QGY-7703 cell line, as well as in gastric cancer (GC) cell and colorectal cancer (CRC) cell. Results In the present work, we observed that CASC2c was significantly down-regulated in HCC tissues and cells. Moreover, its overexpression remarkably inhibited the growth, migration, and invasion of HCC cells in vitro and promoted their apoptosis. Furthermore, we demonstrated that CASC2c overexpression decreased p-ERK1/2 levels in HCC, GC, and CRC cells. Interestingly, while overexpression of CASC2c decreased β-catenin expression in HCC and GC cells, it increased that in CRC cells. Conclusion The lncRNA-CASC2c has a vital role in tumorigenesis and cancer progression, and may serve as a biomarker or therapeutic target in cancer treatment via down-regulation of the ERK1/2 and Wnt/β-catenin signaling pathways.Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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“…miR‐139 can inhibit osteosarcoma cell proliferation and migration through targeting forkhead‐box P2 (Zhong, Liu, Zhang, Luo, & Zheng, ). LncRNA XIST can promote HCC growth by modulating miR‐139‐5p (Mo et al, ). miR‐139 downregulation can contribute to HCC metastasis by inducing c‐Fos (Fan et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…TGF-β1 expression is upregulated in various cancers including colon, gastric, and hepatocellular cancers and can indicate a poor prognosis (Bierie & Moses, 2006). TGF-β1 can increase miR-155 and promote EMT, invasion and metastasis of HCC in vitro (Li, Wang, et al, 2017). miR-199b-5p can attenuate EMT in HCC by targeting TGF-β1 signal (Zhou et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

NEAT1 upregulates TGF‐β1 to induce hepatocellular carcinoma progression by sponging hsa‐mir‐139‐5p

Zhao

et al. 2018

Journal Cellular Physiology

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Increasing evidence has shown that the lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) play important roles in cell proliferation, migration, and invasion in various tumors. In our current study, we concentrated on the biological mechanisms of NEAT1 in hepatocellular carcinoma (HCC) development. It was found that NEAT1 was significantly increased in human HCC cell lines including Hep3B, LM3, MHCC97L, SK-hep1, and HepG2 cells compared to the normal human liver cell line LO2. Meanwhile, we observed that hsa-miR-139-5p was greatly decreased in HCC cells, which suggested a negative correlation between NEAT1 and hsa-mir-139-5p. In addition, NEAT1 downregulation can restrain HCC cell growth, migration, and invasion. Consistently, overexpression of hsa-mir-139-5p exerted a similar phenomenon. Dual-luciferase reporter assay, RIP assay, and RNA pull-down assay confirmed that NEAT1 can function as a ceRNA by sponging hsa-mir-139-5p. In addition, TGF-β1 was identified as a downstream target of hsa-mir-139-5p and hsa-mir-139-5p overexpression was able to suppress TGF-β1 levels. Furthermore, it was indicated that TGF-β1 inhibition can inhibit HCC cell growth, migration, and invasion ability. Taken these together, we speculated that NEAT1 can modulate TGF-β1 expression by sponging hsa-mir-139-5p in HCC. These data indicates that targeting the NEAT1/hsa-mir-139-5p/TGF-β1 axis could be a new strategy for HCC.

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Long non-coding RNA XIST promotes cell growth by regulating miR-139-5p/PDK1/AKT axis in hepatocellular carcinoma

Cited by 76 publications

References 27 publications

XIST promotes gastric cancer (GC) progression through TGF‐β1 via targeting miR‐185

XIST promotes gastric cancer (GC) progression through TGF‐β1 via targeting miR‐185

Long noncoding RNA CASC2c inhibited cell proliferation in hepatocellular carcinoma by inactivated ERK1/2 and Wnt/β-catenin signaling pathway

NEAT1 upregulates TGF‐β1 to induce hepatocellular carcinoma progression by sponging hsa‐mir‐139‐5p

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