<i>Retracted:</i> Epigenetic silenced miR‐125a‐5p could be self‐activated through targeting Suv39H1 in gastric cancer

Cai, Mengxin; Chen, Qiuxian; Shen, Jianjian; Lv, Chenbing; Cai, Lisheng

doi:10.1111/jcmm.13716

Cited by 30 publications

(25 citation statements)

References 26 publications

(103 reference statements)

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“…in human gastric cancer (24), hepatitis B virus-related liver cancer (25) and gastric cancer (26). Notably, a previous report demonstrated that miR-125a-5p expression is downregulated in liver cancer tissues and cell lines, and lowly expressed miR-125a-5p is correlated with aggressive pathological features (27).…”

Section: Microrna-125a-5p Regulates Liver Cancer Cell Growth Migratimentioning

confidence: 94%

“…MiRNAs can act as oncogenes or tumor suppressors in tumor occurrence and progression, including liver cancer ( 21 - 23 ). It was found that miR-125a-5p is a tumor suppressor in the development of various cancers, including in human gastric cancer ( 24 ), hepatitis B virus-related liver cancer ( 25 ) and gastric cancer ( 26 ). Notably, a previous report demonstrated that miR-125a-5p expression is downregulated in liver cancer tissues and cell lines, and lowly expressed miR-125a-5p is correlated with aggressive pathological features ( 27 ).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‑125a‑5p regulates liver cancer cell growth, migration and invasion and EMT by targeting HAX1

Zha

2020

Int J Mol Med

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To date, the role of hematopoietic-substrate-1-associated protein X-1 (HAX1) in liver cancer is rarely studied. The present study explored the role of HAX1 in liver cancer. The association between HAX1 expression and survival of patients with liver cancer was analyzed by a log-rank test. The target genes for HAX1 was predicted by TargetScan and verified by a dual-luciferase reporter assay. The protein and mRNA expressions of HAX1 in liver cancer and adjacent non-cancerous tissues were examined by immunohistochemistry and reverse transcription-quantitative PcR (RT-qPcR). The transfection efficiency of HAX1, small interfering RNA against HAX1, microRNA (miR)-125a mimics, miR-125a inhibitor, miR-223 mimics and miR-223 inhibitor in liver cancer cells was determined by RT-qPcR. The expression of HAX1, p53, VEGF, epithelial-to-mesenchymal transition (EMT)-related markers (E-cadherin, N-cadherin and vimentin) in the cancer cells were determined by western blotting and RT-qPcR. cell viability, migration, invasion and colony formation rates were determined by cell counting Kot-8, wound healing, Transwell and colony formation assays, respectively. The results showed that high expression of HAX1 in liver cancer was found relate to poor prognosis in patients with liver cancer, and upregulation of HAX1 expression in liver cancer tissues was related to lower overall survival. miR-125a-5p directly binds to HAX1. Upregulation of miR-125a-5p expression inhibited cell viability, migration, invasion and colony formation of SK-Hep1 cells and reduced the expression of HAX1, VEGF, N-cadherin and vimentin, but increased cell apoptosis and the expression of p53 and E-cadherin. However, the effects miR-125a-5p upregulation were partially reversed by SK-Hep1 cells with HAX1 overexpression. downregulated miR-125a-5p in SNU-387 cells produced opposite effects, which was partially reversed by HAX silencing. In conclusion, miR-125a-5p suppresses liver cancer growth via targeting HAX1 and concurrently modulating the expression of p53 and VEGF and EMT-related markers.

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Section: Microrna-125a-5p Regulates Liver Cancer Cell Growth Migratimentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

MicroRNA‑125a‑5p regulates liver cancer cell growth, migration and invasion and EMT by targeting HAX1

Zha

2020

Int J Mol Med

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“…The tissue expression level of mir-125a is typically upregulated during differentiation, but is often downregulated in disease states, including diabetic retinopathy and breast cancer (30). Therefore, dysregulated mir-125a expression may be involved in the progression of diseases and can serve as a potential therapeutic target (31,32). The present results suggested that mir-125a expression was downregulated in VSMcs exposed to HG and in aortic media from rats with STZ-induced dM.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑125a‑mediated regulation of the mevalonate signaling pathway contributes to high glucose‑induced proliferation and migration of vascular smooth muscle cells

Lou

et al. 2020

Mol Med Report

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Hyperglycemia contributes to the excessive proliferation and migration of vascular smooth muscle cells (VSMc), which are closely associated with atherosclerosis. Micrornas (mirnas/mirs) constitute a novel class of gene regulators, which have important roles in various pathological conditions. The aim of the present study was to identify mirnas involved in the high glucose (HG)-induced VSMc phenotype switch, and to investigate the underlying mechanism. mirna sequencing and reverse transcription-quantitative Pcr results indicated that inhibition of mir-125a expression increased the migration and proliferation of VSMcs following HG exposure, whereas the overexpression of mir-125a abrogated this effect. Furthermore, dual-luciferase reporter assay results identified that 3-hydroxy-3-methyglutaryl-coa reductase (HMGcr), one of the key enzymes in the mevalonate signaling pathway, is a target of mir-125a. Moreover, HMGcr knockdown, similarly to mir-125a overexpression, suppressed HG-induced VSMc proliferation and migration. These results were consistent with those from the mirna target prediction programs. using a rat model of streptozotocin-induced diabetes mellitus, it was demonstrated that mir-125a expression was gradually downregulated, and that the expressions of key enzymes in the mevalonate signaling pathway in the aortic media were dysregulated after several weeks. in addition, it was found that HG-induced excessive activation of the mevalonate signaling pathway in VSMcs was suppressed following transfection with a mir-125a mimic. Therefore, the present results suggest that decreased mir-125a expression contributed to HG-induced VSMc proliferation and migration via the upregulation of HMGcr expression. Thus, mir-125a-mediated regulation of the mevalonate signaling pathway may be associated with atherosclerosis.dr Yan-ning liu, State Key laboratory for diagnosis and Treatment of infectious diseases, national clinical research center for infectious diseases, collaborative innovation center for diagnosis and Treatment of infectious diseases, The First affiliated

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“…demonstrated that mirna dysfunction participates in cancer progression (19)(20)(21)(22). The role and sequences of mir-4500 have been previously reported (23,24), and the inhibitory effects of mir-4500 on cancer progression have been partially identified (25,26).…”

Section: Long Non-coding Rna Neat1 Modifies Cell Proliferation Colonmentioning

confidence: 97%

Long non‑coding RNA NEAT1 modifies cell proliferation, colony formation, apoptosis, migration and invasion via the miR‑4500/BZW1 axis in ovarian cancer

Sun

Huang

et al. 2020

Mol Med Rep

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ovarian cancer (oc) is a frequently occurring malignant tumor in women. increasing evidence has indicated that long non-coding rna (lncrna) nuclear paraspeckle assembly transcript 1 (neaT1) participates in oc pathogenesis. Thus, the aim of the present study was to explore the function of neaT1 during oc progression. The expression levels of neaT1, microrna (mir)-4500 and basic leucine zipper and W2 domain-containing protein 1 (BZW1) were assessed via reverse transcription-quantitative Pcr and western blotting. Furthermore, cell proliferation, colony formation, apoptosis, migration and invasion were assessed using cell-counting Kit 8, colony formation, flow cytometry and Transwell assays, respectively. cell glycolysis was analyzed using an XF96 metabolic flux analyzer, and the relationship between miR-4500 and NEAT1 or BZW1 was verified via dual-luciferase reporter and rna binding protein immunoprecipitation assays. mir-4500 expression levels were low, whereas neaT1 expression levels were high in oc tissues and cell lines compared with control tissues and cell lines. Moreover, the results indicated that neaT1 was a sponge of mir-4500, which directly targeted BZW1. neaT1 knockdown induced oc cell apoptosis, and inhibited oc cell proliferation, colony formation, migration, invasion and glycolysis. mir-4500 inhibitor reversed neaT1 knockdown-mediated effects. Similarly, mir-4500 mimic-mediated effects on cell functions were reversed by BZW1 overexpression. in addition, the results indicated that BZW1 expression was regulated by neaT1 and mir-4500. collectively, the present study suggested that neaT1 modulated cell proliferation, colony formation, apoptosis, migration, invasion and glycolysis via the mir-4500/BZW1 axis in oc; therefore, neaT1 may serve as a therapeutic target for oc.

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Retracted: Epigenetic silenced miR‐125a‐5p could be self‐activated through targeting Suv39H1 in gastric cancer

Cited by 30 publications

References 26 publications

MicroRNA‑125a‑5p regulates liver cancer cell growth, migration and invasion and EMT by targeting HAX1

MicroRNA‑125a‑5p regulates liver cancer cell growth, migration and invasion and EMT by targeting HAX1

MicroRNA‑125a‑mediated regulation of the mevalonate signaling pathway contributes to high glucose‑induced proliferation and migration of vascular smooth muscle cells

Long non‑coding RNA NEAT1 modifies cell proliferation, colony formation, apoptosis, migration and invasion via the miR‑4500/BZW1 axis in ovarian cancer

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