MicroRNA-370 functions as a tumor suppressor in hepatocellular carcinoma via inhibition of the MAPK/JNK signaling pathway by targeting BEX2

Wang, Xin; Zhu, Weiwei; Xu, Chuanshen; Wang, Feng; Zhu, Xiaodan; Sun, Yandong; Guo, Yuan; Fu, Xiaoyue; Zhang, Yong; Zang, Yunjin

doi:10.1038/s10038-019-0653-x

Cited by 8 publications

(10 citation statements)

References 28 publications

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“…As suggested previously, miR-370 is a neoplasm suppressor via inhibition of the MAPK/JNK signaling pathway by targeting BEX2. 24 The results of the present study further verified that miR-370 inhibits HCC cell migration and proliferation processes. HMGA2 essentially impacts embryogenesis and is an oncoprotein.…”

Section: Discussionsupporting

confidence: 79%

m6A modification of circHPS5 and hepatocellular carcinoma progression through HMGA2 expression

Ding

Chen

et al. 2021

Molecular Therapy - Nucleic Acids

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N6-methyladenosine (m6A) is capable of mediating circRNA generation in carcinoma biology. Nevertheless, the posttranscriptional systems of m6A and circRNA i n hepatocellular carcinoma (HCC) development are still unclear. The present study identified a circRNA with m6A modification, circHPS5, which was increased in neoplasm HCC tissues and indicated poor patient survival. Silencing of circHPS5 inhibited epithelial-mesenchymal transition (EMT) and cancer stem-like cell (CSC) phenotypes. Notably, METTL3 could direct the formation of circHPS5, and specific m6A controlled the accumulation of circHPS5. YTHDC1 facilitated the cytoplasmic output of circHPS5 under m6A modification. In addition, we demonstrated that circHPS5 can act as a miR-370 sponge to regulate the expression of HMGA2 and further accelerate HCC cell tumorigenesis. Accordingly, the m6A modification of circHPS5 was found to modulate cytoplasmic output and increase HMGA2 expression to facilitate HCC development. The new regulatory model of “circHPS5-HMGA2” provides a new perspective for circHPS5 as an important prognostic marker and therapeutic target in HCC and provides mechanistic insight for exploring the carcinogenic mechanism of circHPS5 in HCC.

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Section: Discussionsupporting

confidence: 79%

m6A modification of circHPS5 and hepatocellular carcinoma progression through HMGA2 expression

Ding

Chen

et al. 2021

Molecular Therapy - Nucleic Acids

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“…Previous studies have demonstrated that miR‐370 targets FOXO1, BEX2, or WNK2 and regulates the pathogenesis of cardiac myocytes, hepatocellular carcinoma cells, or breast cancer cells and 17,22,23 . In current study, the luciferase activity analysis confirmed that miR‐370 could bind to 3′‐UTR of SIRT6 mRNA.…”

Section: Discussionsupporting

confidence: 75%

MiR‐370 accelerated cerebral ischemia reperfusion injury via targeting SIRT6 and regulating Nrf2/ARE signal pathway

Ruan

Xie

Gui

et al. 2020

The Kaohsiung J of Med Scie

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Cerebral ischemia reperfusion (CIR) is one of the highly lethal diseases in the world. MicroRNA‐370 (miR‐370) exerts multiple functions in different diseases. However, further research is needed to investigate the potential role of miR‐370 in CIR injury. The in vivo middle cerebral artery occlusion (MCAO) rat model and in vitro oxygen‐glucose deprivation/reoxygenation (OGD/R) SH‐SY5Y cell model were successfully established to mimic CIR injury. The infarct sizes of brain tissues from rats were evaluated. The relationship between miR‐370 and silencing information regulatory protein 6 (SIRT6) was confirmed by luciferase activity assay. The cell viability and apoptosis were determined by CCK‐8 assay and terminal‐deoxynucleoitidyl transferase mediated nick end labeling staining. In this study, miR‐370 was upregulated in brain tissues of MCAO rats and knockdown of miR‐370 decreased cerebral infarction volume of MCAO rats and it alleviated CIR injury in vivo. The in vitro experiments indicated that knockdown of miR‐370 promoted cell viability and alleviated OGD/R‐induced SH‐SY5Y cell apoptosis. Additionally, the TargetScan predicted that SIRT6 was a target of miR‐370 and confirmed by luciferase activity assay. Moreover, miR‐370 inhibited SIRT6 expression and regulated Nrf2/ARE signal pathway, whereas overexpression of SIRT6 partly reversed the effect of miR‐370 on OGD/R‐induced SH‐SY5Y cell injury. Thus, we could conclude that miR‐370 accelerated CIR injury via targeting SIRT6 and regulating Nrf2/ARE signal pathway, which might provide novel therapeutic targets for CIR injury treatment.

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“…Although numerous studies on HCC have been carried out for years, the molecular mechanisms of its genesis, development and metastasis have yet to be fully elucidated. It has been reported that microRNAs played an important role in suppressing the development of hepatocellular carcinoma [14]. Growing evidence has demonstrated that let-7 acts as a tumor suppressor in various cancers.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA let-7b inhibits cell proliferation via upregulation of p21 in hepatocellular carcinoma

Fang

Yuan

et al. 2020

Cell Biosci

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Background: Hepatocellular carcinoma (HCC) is one of the most malignant tumor types and has a high incidence and mortality. Many miRNAs play important roles in the development of HCC. Identification of these miRNAs and their targets is increasingly urgent for a better understandingof miRNA function in both physiological and pathological contexts. Many studies have shown that the expression of let-7 is often downregulated in the process of tumorigenesis, suggesting that let-7 may participate in this process as an oncogene. Methods: Immunochemistry staining was used to observe the expression of let-7b in HCC tissues. A CCK-8 assay was employed to detect the role of let-7b in the proliferation of HCC cells. The cell cycle of HCC cells was examined by flow cytometry. BALB/c nu/nu mice were used to detect the tumorigenesis potential of HCC cells; western blot and real-time PCR were employed to observe the expression of p21 in HCC cells. Results: In our previous studies investigating HCC tissue samples obtained from the national tissue samples bank of liver cancer in Eastern Hepatobiliary Surgery Hospital, we found one abnormal expression of miRNA (let-7b), which was significantly downregulated in HCC tissue. In the current work, we studied the relationship between let-7b and HCC to potentially provide invaluable information for developing novel therapeutic strategies for treating HCC. Based on our findings, let-7b expression was absent in HCC tumors, and its lower expression was associated with poor prognosis of HCC. In further experiments, we found that let-7b inhibited HCC cell proliferation through upregulation of p21. Conclusion: The results of our study suggested that let-7b might inhibit the proliferation of HCC cells by upregulating p21.

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MicroRNA-370 functions as a tumor suppressor in hepatocellular carcinoma via inhibition of the MAPK/JNK signaling pathway by targeting BEX2

Cited by 8 publications

References 28 publications

m6A modification of circHPS5 and hepatocellular carcinoma progression through HMGA2 expression

m6A modification of circHPS5 and hepatocellular carcinoma progression through HMGA2 expression

MiR‐370 accelerated cerebral ischemia reperfusion injury via targeting SIRT6 and regulating Nrf2/ARE signal pathway

MicroRNA let-7b inhibits cell proliferation via upregulation of p21 in hepatocellular carcinoma

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