RETRACTED ARTICLE: MicroRNA-325-3p inhibits cell proliferation and induces apoptosis in hepatitis B virus-related hepatocellular carcinoma by down-regulation of aquaporin 5

Zhang, Zhitao; Han, Yanzhen; Sun, Guangxin; Liu, Xiaohong; Jia, Xiaoyan; Yu, Xiangjun

doi:10.1186/s11658-019-0137-1

Cited by 45 publications

(32 citation statements)

References 43 publications

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“…Hsa-miR-325 and hsa-miR-510-5p participate in tumor development (40)(41)(42)(43). Hsa-miR-325 has been identified as a potential biomarker in human bladder cancer and low expression of hsa-miR-325 was associated with poor overall survival in patients with bladder cancer (40).…”

Section: Discussionmentioning

confidence: 99%

“…Hsa-miR-325 has been identified as a potential biomarker in human bladder cancer and low expression of hsa-miR-325 was associated with poor overall survival in patients with bladder cancer (40). In addition, downregulation of hsa-miR-325 has been demonstrated to promote the progression of non-small cell lung cancer and HCC (41,42). Chen et al (43) found that hsa-miR-510-5p acted as a tumor suppressor in renal cell carcinoma by reducing cell proliferation, migration and inducing apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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TMEM206 is a potential prognostic marker of hepatocellular carcinoma

et al. 2020

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Transmembrane proteins are involved in the transportation of materials into and out of cells. The transmembrane protein (TMEM) family is a collection of poorly described transmembrane proteins that serve important roles in tumor development and progression. A number of TMEM proteins have been discovered. A newly discovered TMEM protein, TMEM206, transports ions across the membrane under physiological and pathological conditions, generating an acidic environment, which serves an important role in the microenvironment. However, the prognostic value and regulatory mechanisms of action of TMEM206 in tumors is unclear. The aim of the present study was to evaluate the prognostic value and regulation mechanisms of TMEM206 in tumors. Firstly, the expression of TMEM206 in tumors and normal tissues was assessed using the GEPIA and Oncomine databases and the results revealed that TMEM206 expression increased or decreased depending on the type of tumor. Subsequently, using the Human Protein Atlas and the Kaplan-Meier plotter, the findings of the present study revealed that TMEM206 is related to the prognosis of hepatocellular carcinoma. In order to explore the mechanism of TMEM206 in promoting tumor progression, GEO and cBioPortal were used to determine genes that may be co-expressed with TMEM206. MetaScape was used to identify the signaling pathways that TMEM206 may participate in. Finally, miRWalk, miRDB and TargetScan were used to identify miRNAs that may regulate the expression of TMEM206 and the findings revealed that 2 miRNA (hsa-miR-325 and hsa-miR-510-5p) were involved. In conclusion, upregulation of TMEM206 is associated with poor prognosis in patients with hepatocellular carcinoma.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

TMEM206 is a potential prognostic marker of hepatocellular carcinoma

et al. 2020

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“…Previous studies demonstrated that miR-325-3p was implicated in cellular processes in different types of diseases. For example, Zhang et al (21) reported that miR-325-3p decreases aquaporin 5 expression to confine hepatitis B virus replication in hepatocellular carcinoma. Another study investigating hypoxic-ischemic brain damage indicated that miR-325-3p aggravates rat neonatal hypoxia-ischemia brain injury by modulating aralkylamine N-acetyltransferase (22).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA MEG3 knockdown alleviates hypoxia‑induced injury in rat cardiomyocytes via the miR‑325‑3p/TRPV4 axis

Zhou¹,

Li²,

Zhao³

et al. 2020

Mol Med Rep

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Acute myocardial infarction (AMI) is a common cardiac disease. Long non-coding RNA maternally expressed 3 (MEG3) is associated with cellular processes in numerous complicated diseases, including AMI. However, the mechanism underlying MEG3 in myocardial hypoxia is not completely understood. The present study aimed to investigate the underlying mechanism of MEG3 in myocardial hypoxia. The expression levels of hypoxia-inducible factor 1α (HIF1α), MEG3, microRNA (miR)-325-3p, and transient receptor potential cation channel subfamily V member 4 (TRPV4) in hypoxia-treated H9c2 cells were detected via reverse transcription-quantitative PCR. The protein expression levels of HIF1α, Bcl-2, Bax, cleaved caspase-3 and TRPV4 were detected via western blotting. Cell viability and apoptosis were assessed by performing an MTT assay and flow cytometry, respectively. Lactate dehydrogenase (LDH) release was monitored by conducting an LDH determination assay. The Dual-Luciferase reporter assay was performed to verify the targeted relationship between miR-325-3p and MEG3 or TRPV4. The expression levels of MEG3 and TRPV4 were significantly increased, whereas miR-325-3p expression levels were significantly decreased in hypoxic H9c2 cells compared with normoxic H9c2 cells. In addition, miR-325-3p was downregulated by MEG3 compared with the vector group, and miR-325-3p targeted TRPV4 in hypoxia-treated H9c2 cells. The results indicated that MEG3 knockdown attenuated hypoxia-stimulated injury in H9c2 cells by regulating miR-325-3p. TRPV4 knockdown also mitigated hypoxia-induced injury in H9c2 cells via miR-325-3p. Furthermore, compared with the vector group, MEG3 increased TRPV4 expression in hypoxia-treated H9c2 cells by sponging miR-325-3p. Collectively, the results of the present study suggested that MEG3 modulated TRPV4 expression to aggravate hypoxia-induced injury in rat cardiomyocytes by sponging miR-325-3p.

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“…miRNAs are endogenous, non-coding small RNAs which participate in posttranscriptional regulation by targeting the 3'-untranslated region (UTR) of mRNAs, causing degradation or translation suppressing of mRNAs, and act as suppressors or oncogenes in tumorigenesis [49][50]. In this study, miRNAs which may influence GOLGA8B expression were selected only when they were predicted by six algorithms.…”

Section: Discussionmentioning

confidence: 99%

Clinical Value and Potential Mechanisms Exploration of GOLGA8B in Hepatocellular Carcinoma: A Comprehensive Investigation Based on Real-Time Quantitative Polymerase Chain Reaction, RNA-seq, Microarray and Immunohistochemistry

Ma¹,

Zhai²,

Wu³

et al. 2019

Preprint

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Introduction Recent studies found that GOLGA8B plays an essential role in different cancers. However, the role GOLGA8B plays in the carcinogenesis and development of hepatocellular carcinoma (HCC) remains unclear. This study explores the clinical significance and prospective mechanisms of GOLGA8B in HCC. Materials and methods The expression of GOLGA8B was detected in tissues of HCC and non-HCC controls. A real-time quantitative polymerase chain reaction analysis was performed to evaluate the mRNA expression of GOLGA8B. RNA-sequencing data and microarray chip data were obtained for further analysis. The role GOLGA8B plays in patients with HCC was also evaluated. An immunohistochemistry (IHC) analysis was also performed to evaluate the protein expression of GOLGA8B. The different GOLGA8B expression resources, including mRNA and protein expression, were integrated by calculating standard mean difference (SMD) and summary of the receiver operator characteristic (sROC). Genes co-expressed GOLGA8B were predicted. Enrichment analyses including Gene ontology (GO) and biological pathway were performed to investigate the essential molecular mechanisms. Hub genes were screened out by a protein-protein interactions network. MicroRNAs which target GOLGA8B at a posttranscriptional level were also predicted. Results According to different resources, GOLGA8B manifested a higher expression in tissues of HCC than in non-HCC controls and exhibited clinical values for HCC. The RT-qPCR analysis revealed an increasing trend of GOLGA8B expression in HCC. GOLGA8B expresssion was significantly increased in RNA-sequencing and 7 of 13 microarray chip. IHC analysis also revealed significantly higher expression of GOLGA8B protein. Moreover, GOLGA8B expression was correlated with pathologic tumors and stages according to RNA-sequencing data and IHC analysis. The integrated SMD and sROC of different resources was 0.893 (P=0.004) and 0.79. A total 1303 co-expressed genes were gathered to perform enrichment analyses. The most significant biological pathways of co-expressed genes were spliceosome and mitogen-activated protein kinase signalling (MAPK). Four hub genes (SF3B1, HNRNPA2B1, HNRNPA1 and SRRM2) and five miRNAs (miR-369-3p, miR-203a, miR-374b-5p, miR-139-5p and miR-144-3p) were screened out. Conclusion GOLGA8B expression was increased in HCC and may serve as a novel target for HCC diagnosis and treatment.

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RETRACTED ARTICLE: MicroRNA-325-3p inhibits cell proliferation and induces apoptosis in hepatitis B virus-related hepatocellular carcinoma by down-regulation of aquaporin 5

Cited by 45 publications

References 43 publications

TMEM206 is a potential prognostic marker of hepatocellular carcinoma

TMEM206 is a potential prognostic marker of hepatocellular carcinoma

Long non‑coding RNA MEG3 knockdown alleviates hypoxia‑induced injury in rat cardiomyocytes via the miR‑325‑3p/TRPV4 axis

Clinical Value and Potential Mechanisms Exploration of GOLGA8B in Hepatocellular Carcinoma: A Comprehensive Investigation Based on Real-Time Quantitative Polymerase Chain Reaction, RNA-seq, Microarray and Immunohistochemistry

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