Influence of miR‐520e‐mediated <scp>MAPK</scp> signalling pathway on <scp>HBV</scp> replication and regulation of hepatocellular carcinoma cells via targeting EphA2

Tian, Jing-hui; Li, Wendong; Zhang, Zhiyong; Tang, Lihua; Liu, Dong; Tian, Zhong; Lin, Shaowei; Li, Yingjie

doi:10.1111/jvh.13048

Cited by 13 publications

(12 citation statements)

References 43 publications

(78 reference statements)

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“…Wang et al [ 51 ] showed that miR-302a inhibits cell proliferation and promotes the apoptosis of human HCC cells by targeting MAP3K2 and PBX3 to reduce the expression of the key MAPK-associated proteins, including phosphorylated ERK (p-ERK1/2), p38 (p-p38), and JNK (p-JNK). Further, Tian et al [ 52 ] demonstrated that a decrease in miR-520e expression was observed in HBV-positive HCC cells and tissues. Further studies have revealed that miR-520e overexpression specifically inhibited EPH receptor A2 (EphA2), thereby blocking the p38 MAPK and ERK1/2 signaling pathways.…”

Section: Microrna Related To the Mapk Signaling Pathway In Liver Cancermentioning

confidence: 99%

Non-Coding RNA Related to MAPK Signaling Pathway in Liver Cancer

Wang

Feng

Tang

2022

IJMS

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The advancement in high-throughput sequencing analysis and the evaluation of chromatin state maps have revealed that eukaryotic cells produce many non-coding transcripts/RNAs. Further, a strong association was observed between some non-coding RNAs and cancer development. The mitogen-activated protein kinases (MAPK) belong to the serine–threonine kinase family and are the primary signaling pathways involved in cell proliferation from the cell surface to the nucleus. They play an important role in various human diseases. A few non-coding RNAs associated with the MAPK signaling pathway play a significant role in the development of several malignancies, including liver cancer. In this review, we summarize the molecular mechanisms and interactions of microRNA, lncRNA, and other non-coding RNAs in the development of liver cancer that are associated with the MAPK signaling pathway. Further, we briefly discuss the therapeutic strategies for liver cancer related to ncRNA and the MAPK signaling pathway.

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Section: Microrna Related To the Mapk Signaling Pathway In Liver Cancermentioning

confidence: 99%

Non-Coding RNA Related to MAPK Signaling Pathway in Liver Cancer

Wang

Feng

Tang

2022

IJMS

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“…EPHA2 has been reported to be associated with mitogen activated protein kinase (MAPK) pathways. Jing-Hui et al reported that overexpression of microRNA miR-520e inhibited p38MAPK and ERK1/2 signaling pathways through inhibition of EPHA2, ultimately leading to the suppression of cell proliferation in hepatocellular carcinoma [ 31 ]. EPHA2 is able to induce EMT in gastric cancer [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

MFSD4A inhibits the malignant progression of nasopharyngeal carcinoma by targeting EPHA2

et al. 2022

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DNA Methylation can lead to abnormal gene expression. In the present study, we investigated whether the expression of methylated MFSD4A (major facilitator superfamily domain containing 4 A) was downregulated in nasopharyngeal carcinoma (NPC) and whether it is associated with malignant progression and poor prognosis of NPC. Bioinformatic analysis, bisulfite pyrosequencing, quantitative real-time reverse transcription PCR, and western blotting assays were performed to explore the relationship between hypermethylation of MFSD4A and its expression in NPC. The role of MFSD4A in NPC was verified by Cell Cycle Kit 8, transwell assays and flow cytometry in vitro and by animal experiments in vivo. Mass spectrometry, co-immunoprecipitation, and immunofluorescence assays were applied to explore the mechanism by which MFSD4A inhibits NPC. The prognostic significance of MFSD4A or EPHA2 was investigated by immunohistochemical analysis of clinical specimens. Hypermethylation of the promoter region of MFSD4A led to decreased expression of MFSD4A. When MFSD4A expression was upregulated or downregulated, the proliferation, apoptosis, migration, and invasion abilities of NPC cells were altered accordingly. Mechanistically, MFSD4A could specifically bind to and degrade EPH receptor A2 (EPHA2) by recruiting ring finger protein 149 (RNF149), which led to alterations in the EPHA2-mediated PI3K-AKT-ERK1/2 pathway and epithelial-mesenchymal transition (EMT), thereby affecting NPC progression. Clinically, high MFSD4A expression or low-EPHA2 expression was associated with better prognosis for patients with NPC. In all, reduced MFSD4A expression in NPC is caused by promoter hypermethylation. MFSD4A or EPHA2 expression is associated with the malignant biological behavior and prognosis of NPC. MFSD4A is a promising potential therapeutic target for NPC.

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“…Promoted EPHA2 expression in cancer cells is linked to a dismal prognosis because of recurrence as a consequence of enhanced metastasis [28]. As for its upstream miRNAs, EPHA2 has been indicated to be targeted by different miRNAs to participate the development of various cancers, including non-small cell lung cancer [29], hepatocellular carcinoma [30] as well as colorectal cancer [31]. After the validation of the targeting relationship between EPHA2 and miR-451a in BCa cells, we carried out rescue experiments again.…”

Section: Discussionmentioning

confidence: 99%

microRNA-451a promoter methylation regulated by DNMT3B expedites bladder cancer development via the EPHA2/PI3K/AKT axis

et al. 2020

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Background The downregulation of microRNA (miR)-451a has been reported in bladder cancer (BCa) tissues. Herein, we elucidated the role of miR-451a in BCa with the involvement of DNA methyltransferase 3B (DNMT3B). Methods We first screened the differentially expressed miRNAs from the serum of 12 BCa patients and 10 healthy controls in the BCa database GSE113486. Subsequently, we detected miR-451a expression and CpG island methylation of the promoter in BCa cells T24 and 5637 with DNMT3B knockdown. The downstream mRNAs of miR-451a were predicted by bioinformatics and KEGG enrichment analysis. Afterwards, the expression patterns of DNMT3B, miR-451a and erythropoietin-producing hepatocellular receptor tyrosine kinase class A2 (EPHA2) were altered in BCa cells to test the ability of cell proliferation, apoptosis, migration as well as invasion. Finally, the effect of miR-451a and DNMT3B was evaluated in vivo. Results miR-451a was significantly reduced in serum of BCa patients and cell lines. Moreover, the expression of DNMT3B in BCa cells was significantly increased, thus promoting methylation of the miR-451a promoter, resulting in miR-451a inhibition. Additionally, we found that miR-451a targeted and negatively regulated EPHA2, while EPHA2 could activate the PI3K/AKT signaling, driving BCa cell growth and metastasis. Conclusions Our study proposed and demonstrated that miR-451a downregulation mediated by DNMT3B is critical for proliferation, migration, and invasion of BCa, which may be beneficial for developing more effective therapies against BCa.

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Influence of miR‐520e‐mediated MAPK signalling pathway on HBV replication and regulation of hepatocellular carcinoma cells via targeting EphA2

Cited by 13 publications

References 43 publications

Non-Coding RNA Related to MAPK Signaling Pathway in Liver Cancer

Non-Coding RNA Related to MAPK Signaling Pathway in Liver Cancer

MFSD4A inhibits the malignant progression of nasopharyngeal carcinoma by targeting EPHA2

microRNA-451a promoter methylation regulated by DNMT3B expedites bladder cancer development via the EPHA2/PI3K/AKT axis

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