Function and clinical potential of microRNAs in hepatocellular carcinoma

Wang, Limin; Yue, Yongfang; Wang, Xian; Jin, Hongchuan

doi:10.3892/ol.2015.3759

Cited by 24 publications

(17 citation statements)

References 157 publications

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“…Identifying the biomarker proteins and their regulating miRNAs that are essential for HCC progression may provide promising therapeutic opportunities. Many miRNAs have been found to be dysregulated in HCC and function as oncogenes or tumor suppressors, depending on their targets in HCC tumorigenesis . Recently, studies have found that miR‐24 acts as an oncogene in several tumors, including HCC .…”

Section: Discussionmentioning

confidence: 99%

“…Many miRNAs have been found to be dysregulated in HCC and function as oncogenes or tumor suppressors, depending on their targets in HCC tumorigenesis. 3,[9][10][11][12] Recently, studies have found that miR- It is generally accepted that miRNAs exert their function through regulating the expression of their downstream target genes. In this study, we identified MT1M as a target of miR-24-3p in HCC.…”

Section: Discussionmentioning

confidence: 99%

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MiR‐24‐3p enhances cell growth in hepatocellular carcinoma by targeting metallothionein 1M

Dong

Ding

et al. 2016

Cell Biochemistry & Function

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Dysregulation of microRNAs has been demonstrated to contribute to malignant progression of cancers, including hepatocellular carcinoma (HCC). MiR-24-3p was previously reported to be significantly upregulated in HCC. However, the potential role and mechanism of action of miR-24-3p in the initiation and progression of HCC remain largely unknown. Quantitative reverse transcription polymerase chain reaction demonstrated that miR-24-3p was significantly upregulated in HCC tumor tissues compared with nontumor tissues. The cell viability, colony formation assay, and tumorigenicity assays in nude mice showed that miR-24-3p could enhance HCC cell growth in vitro and in vivo. Metallothionein 1M was verified as an miR-24-3p target gene by using dual-luciferase reporter assays, quantitative reverse transcription polymerase chain reaction, and Western blotting, which was involved in miR-24-3p regulated HCC cell growth. These results indicated that miR-24-3p plays an important role in the initiation and progression of HCC by targeting metallothionein 1M, and the miR-24-3p/metallothionein 1M pathway may contribute to the development of novel therapeutic strategies for HCC in the future.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MiR‐24‐3p enhances cell growth in hepatocellular carcinoma by targeting metallothionein 1M

Dong

Ding

et al. 2016

Cell Biochemistry & Function

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“…In addition, miR-34a showed tumor suppressor effects by reducing cell migration and invasion via targeting the hepatocyte growth factor (HGF) receptor c-MET. In contrast, miR-21 represented an oncogenic miRNA in HCC that induce cell growth, invasion, and metastasis by inhibiting PTEN gene activity (13).…”

Section: Editorialmentioning

confidence: 99%

MicroRNAs are key regulators of hepatocellular carcinoma (HCC) cell dissemination—what we learned from microRNA-494

González-Vallinas

Breuhahn

2016

Hepatobiliary Surg. Nutr.

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“…The increased de novo FAS in cancer cells occurs through multiple mechanisms, most of which involve the abnormal expression of key lipogenic enzymes and miRNAs. miRNAs play an important role in HBV‐induced lipid metabolism disorders and HBV‐related liver diseases .…”

Section: Introductionmentioning

confidence: 99%

Pleiotrophin, a target of miR‐384, promotes proliferation, metastasis and lipogenesis in HBV‐related hepatocellular carcinoma

Bai

Xia

Sun

et al. 2017

J Cellular Molecular Medi

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Hepatitis B virus (HBV) infection plays a crucial role and is a major cause of hepatocellular carcinoma (HCC) in China. microRNAs (miRNAs) have emerged as key players in hepatic steatosis and carcinogenesis. We found that down‐regulation of miR‐384 expression was a common event in HCC, especially HBV‐related HCC. However, the possible function of miR‐384 in HBV‐related HCC remains unclear. The oncogene pleiotrophin (PTN) was a target of miR‐384. HBx inhibited miR‐384, increasing PTN expression. The PTN receptor N‐syndecan was highly expressed in HCC. PTN induced by HBx acted as a growth factor via N‐syndecan on hepatocytes and further promoted cell proliferation, metastasis and lipogenesis. PTN up‐regulated sterol regulatory element‐binding protein 1c (SREBP‐1c) through the N‐syndecan/PI3K/Akt/mTORC1 pathway and the expression of lipogenic genes, including fatty acid synthesis (FAS). PTN‐mediated de novo lipid synthesis played an important role in HCC proliferation and metastasis. PI3K/AKT and an mTORC1 inhibitor diminished PTN‐induced proliferation, metastasis and lipogenesis. Taken together, these data strongly suggest that the dysregulation of miR‐384 could play a crucial role in HBV related to HCC, and the target gene of miR‐384, PTN, represents a new potential therapeutic target for the prevention of hepatic steatosis and further progression to HCC after chronic HBV infection.

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Function and clinical potential of microRNAs in hepatocellular carcinoma

Cited by 24 publications

References 157 publications

MiR‐24‐3p enhances cell growth in hepatocellular carcinoma by targeting metallothionein 1M

MiR‐24‐3p enhances cell growth in hepatocellular carcinoma by targeting metallothionein 1M

MicroRNAs are key regulators of hepatocellular carcinoma (HCC) cell dissemination—what we learned from microRNA-494

Pleiotrophin, a target of miR‐384, promotes proliferation, metastasis and lipogenesis in HBV‐related hepatocellular carcinoma

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