miR-425-5p Acts as a Molecular Marker and Promoted Proliferation, Migration by Targeting RNF11 in Hepatocellular Carcinoma

Rao, Dan; Guan, Songmei; Huang, Jun; Chang, Qing; Duan, Shigang

doi:10.1155/2020/6530973

Cited by 13 publications

(11 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been previously found that miR-425 regulated the proliferation, invasion and metastasis of hepatocellular carcinoma cells ( 36 ). These results are consistent with the previous findings that miR-425 can improve cell survival and is associated with a poor outcome ( 37 , 38 ). Overexpression of miR-425 promotes cell proliferation and migration via targeting RNF11 in HCC and it can also bind with FOXD3 to promote cell migration and invasion ( 36 , 37 ).…”

Section: Discussionsupporting

confidence: 93%

“…These results are consistent with the previous findings that miR-425 can improve cell survival and is associated with a poor outcome ( 37 , 38 ). Overexpression of miR-425 promotes cell proliferation and migration via targeting RNF11 in HCC and it can also bind with FOXD3 to promote cell migration and invasion ( 36 , 37 ). These results suggested that miR-425 is an oncogene to promote tumor progression.…”

Section: Discussionsupporting

confidence: 93%

See 1 more Smart Citation

miR‑425 regulates lipophagy via SIRT1 to promote sorafenib resistance in liver cancer

et al. 2021

View full text Add to dashboard Cite

Liver cancer is one of the most malignant cancer, with poor outcomes and a high incidence rate, and current treatment approaches to prevent tumor progression and development remain unsatisfactory. Therefore, it is urgent to explore novel methods to inhibit tumor growth and metastasis. Autophagy is a highly conserved process associated with metastasis and drug resistance. Lipids are selectively recognized and degraded via autophagy; thus, autophagy is a crucial process to maintain tumor self-protection. MicroRNA (miR)-425 is a tumor-associated gene involved in liver cancer development that can induce cell proliferation and drug resistance. Using Cell Counting Kit-8 assays, western blot analysis and immunofluorescence assays, the present study revealed that inhibition of miR-425 promoted lipophagy by mediating the autophagy process, which in turn helps to promote sorafenib resistance. Using a bioinformatics website, it was revealed that autophagy promoted lipophagy by targeting silent information regulator 2 homolog 1 (SIRT1). The results of luciferase reporter assays supported this finding, and rescue experiments provided additional evidence. Overall, the current results suggested that inhibition of miR-425 expression increased SIRT1 expression to promote lipophagy, leading to the inhibition of liver cancer cell proliferation.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

miR‑425 regulates lipophagy via SIRT1 to promote sorafenib resistance in liver cancer

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Previous studies have reported that miR-362-3p/miR-425-5p exerts oncogenic effects by regulating HCC proliferation and migration. For example, miR-425-5p achieved its role in promoting the malignant progression of HCC by regulating RNF11 and was seen as a molecular target to predict the outcome of HCC patients [ 20 ]. Upregulation of miR-362-3p, which targets and regulates Tob2, thereby promoting the proliferation of hepatocellular carcinoma cells [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Downregulation of ZC3H13 by miR-362-3p/miR-425-5p is associated with a poor prognosis and adverse outcomes in hepatocellular carcinoma

Liu

Cao

et al. 2022

Aging

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) is notorious for its poor prognosis. Previous studies identified several N6methyladenosine (m6A)-related genes that play key roles in the initiation and progression of HCC patients. In particular, the N6-methyladenosine RNA methylation regulator ZC3H13 could be a candidate as a novel biomarker and therapeutic target for hepatocellular carcinoma. In HCC, low expression of ZC3H13 was reported, but the molecular reason is unclear. In this study, we performed pan cancer analysis for ZC3H13 expression and prognosis using The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data and found that ZC3H13 might be a potential tumor suppressor gene in HCC. Subsequently, miRNAs contributing to ZC3H13 downregulation were identified by a series of in silico analyses, including expression analysis, correlation analysis, and survival analysis. Finally, the miR-362-3p/miR-425-5p-ZC3H13 axis was identified as the most likely upstream miRNA-related pathway of ZC3H13 in HCC. Additionally, miR-362-3p/miR-425-5p mimic and inhibitor results were detected by quantitative real-time PCR (qPCR) analysis and western blotting. We identified an upstream regulatory mechanism of ZC3H13 in HCC, namely, the miR-362-3p/miR-425-5p-ZC3H13 axis. Moreover, the ZC3H13 level was significantly positively associated with tumor immune cell infiltration, biomarkers of immune cells, and immune checkpoint expression. Collectively, our findings elucidated that ncRNA-mediated downregulation of ZC3H13 was correlated with a poor prognosis and tumor immune infiltration in HCC. In conclusion, this study demonstrates that ZC3H13 is a direct target of miR-362-3p/miR-425-5p in liver hepatocellular carcinoma (LIHC) that regulates immune modulation in the microenvironment of LIHC.

show abstract

“…Our results indicated that silencing miR-425-5p inhibited the proliferation, migration, and invasion of OC cells, which was consistent with its role in other cancers. For example, miR-425-5p is significantly increased in hepatocellular carcinoma (HCC) tissues and is closely related to the poor prognosis of patients with HCC, which as an oncogene promotes the proliferation and migration of HCC cells via RNF11 or FOXD3 [ 18 , 19 ]. In colorectal cancer, miR-425-5p promotes cell proliferation, migration, invasion, and EMT by activating the CTNND1 -mediated β-catenin pathway [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-425-5p accelerated the proliferation, migration, and invasion of ovarian cancer cells via targeting AFF4

Guo

Zhang³

et al. 2021

J Ovarian Res

View full text Add to dashboard Cite

Background Accumulating data have established that microRNAs (miRNAs) play significant regulatory roles in the carcinogenesis and progression of ovarian cancer (OC). MiR-425-5p was reported to function in various tumors. However, the roles and underlying mechanism of miR-425-5p involvement in OC development and progression are unclear. Methods A comprehensive strategy of data mining, computational biology, and real-time polymerase chain reaction was employed to identify the involvement of miR-425-5p in OC progression. The effect of miR-425-5p on the proliferation, migration, and invasion of OC cells was determined using Cell Counting Kit-8, wound-healing, and Matrigel invasion assays, respectively. Luciferase assay was performed to evaluate the interactions between miR-425-5p and MAGI2-AS3 or AFF4. Results miR-425-5p was significantly up-regulated in OC tissues and cells. The luciferase reporter assay revealed that miR-425-5p was negatively regulated by MAGI2-AS3. Silencing miR-425-5p inhibited the proliferation, migration, and invasion of OC cells in vitro. Bioinformatics analysis and luciferase reporter assay revealed that AFF4 was the target gene of miR-425-5p. Moreover, AFF4 expression was significantly decreased in OC and was closely related to the good prognosis of patients with OC. AFF4 overexpression inhibited the proliferation, migration, and invasion of OC cells in vitro. By contrast, silencing AFF4 promoted the proliferation, migration, and invasion of OC cells in vitro. Finally, AFF4 suppression rescued the inhibitory effect of silencing miR-425-5p on the proliferation, migration, and invasion of OC cells. Conclusion To the best our knowledge, this is the first study to demonstrate that miR-425-5p overexpression in OC is negatively regulated by MAGI2-AS3. Moreover, miR-425-5p promotes the proliferation, migration, and invasion of OC cells by targeting AFF4, suggesting that miR-425-5p/AFF4 signaling pathway represented a novel therapeutic target for patients with OC.

show abstract

miR-425-5p Acts as a Molecular Marker and Promoted Proliferation, Migration by Targeting RNF11 in Hepatocellular Carcinoma

Cited by 13 publications

References 40 publications

miR‑425 regulates lipophagy via SIRT1 to promote sorafenib resistance in liver cancer

miR‑425 regulates lipophagy via SIRT1 to promote sorafenib resistance in liver cancer

Downregulation of ZC3H13 by miR-362-3p/miR-425-5p is associated with a poor prognosis and adverse outcomes in hepatocellular carcinoma

MiR-425-5p accelerated the proliferation, migration, and invasion of ovarian cancer cells via targeting AFF4

Contact Info

Product

Resources

About