miR-502 inhibits cell proliferation and tumor growth in hepatocellular carcinoma through suppressing phosphoinositide 3-kinase catalytic subunit gamma

Chen, Suling; Li, Fang; Chai, Hai-yun; Xin, Tao; Wang, Haili; Ji, Ai‐Fang

doi:10.1016/j.bbrc.2015.06.168

Cited by 22 publications

(14 citation statements)

References 28 publications

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“…In addition, we previously confirmed the tumour‐suppressing role of a series of miRNAs, including miR‐22, miR‐148a‐3p, miR‐182‐5p, miR‐320c, miR‐323a‐3p, miR‐409, miR‐433 and miR‐576, which are involved in regulating oncogenicity and progression of BCa . MiR‐502‐5p is located at Xp11.23 and has been reported to be associated with the tumorigenicity and progression of breast cancer, colon cancer, liver cancer and non‐Hodgkin lymphoma . However, the extract role of miR‐502‐5p in bladder cancer has not been investigated.…”

Section: Introductionsupporting

confidence: 58%

CCND1, NOP14 and DNMT3B are involved in miR‐502‐5p–mediated inhibition of cell migration and proliferation in bladder cancer

Ying

Xie

et al. 2020

Cell Proliferation

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Objectives Downregulation of miR‐502‐5p has emerged as a critical factor in tumour progression in several cancers. Herein, we elucidated the role of miR‐502‐5p in bladder cancer. Materials and methods RT‐qPCR was performed to examine the expression of miR‐502‐5p in bladder cancer. And DNA methylation analysis showed that epigenetic mechanisms may contribute to the downregulation of miR‐502‐5p. Then, wound‐healing assay, transwell assay, colony formation assay, CCK8 assay and flow cytometry analysis were applied to evaluate the function of miR‐502‐5p in bladder cancer cell lines. Western blot was conducted to measure the protein levels of related genes. Furthermore, dual‐luciferase reporter assay, in vivo tumorigenesis assay and immunohistochemical staining were also conducted as needed. Results MiR‐502‐5p is frequently downregulated in BCa. Meanwhile, hypermethylation of CpG islands contributes to the downregulation of miR‐502‐5p. Functionally, overexpression of miR‐502‐5p inhibited cell proliferation and migration in vitro and repressed tumour growth in vivo. CCND1, DNMT3B and NOP14 were identified as direct targets of miR‐502‐5p. Interestingly, DNMT3B and miR‐502‐5p established a positive feedback loop in the regulation of bladder cancer. In addition, rescue experiments further validated the direct molecular interaction between miR‐502‐5p and its targets. Conclusions Our study proposed and demonstrated that the miR‐502‐5p–mediated regulatory network is critical in bladder cancer; this network may be useful in the development of more effective therapies against bladder cancer.

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Section: Introductionsupporting

confidence: 58%

CCND1, NOP14 and DNMT3B are involved in miR‐502‐5p–mediated inhibition of cell migration and proliferation in bladder cancer

Ying

Xie

et al. 2020

Cell Proliferation

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“…Combining with the previous reports, these observations further confirmed the oncogenic roles of PIK3R1 in HCC. The downregulation of PIK3R1 led to growth inhibition of HCC cells, which might be correlated with cell arrest in G2/M phase of cell cycle and apoptosis enhancement [ 14 , 15 ]. As we know, PI3K is a dimeric enzyme consisting of a catalytic (p110) and a regulatory subunit (p85α).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of PIK3R1 promotes hepatocellular carcinoma progression

Xiang

Huang

et al. 2018

Biol Res

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BackgroundPhosphoinositide-3-kinase, regulatory subunit 1 (PIK3R1) could regulate cancer cell proliferation important for cancer cell proliferation; however, its role in Hepatocellular carcinoma (HCC) remains largely unknown. Here, we investigated the role of PIK3R1 in HCC and examined the underlying molecular mechanisms.MethodsThe expression of PIK3R1 was evaluated by immunohistochemistry and qRT-PCR in a series of HCC tissues. The mRNA and protein expression of PIK3R1 was used by qRT-PCR and western blot assays in a series of human HCC cell lines, and then we choose MHCC97H and HCCLM3 cells as a model to investigate the effect of PIK3R1 on HCC progression. The effects of PIK3R1 knowdown on cell proliferation, migration, apoptosis of HCC were assessed by the MTT assay, clonogenic assays, wound healing assay and flow cytometry in vitro. Western blot assay was performed to assess the expression changes of PI3K/AKT/mTOR signaling pathway.ResultsOur results found that PIK3R1 was highly expressed in HCC tissues compared with adjacent normal tissues. Knockdown of PIK3R1 inhibited the proliferation, migration and promoted apoptosis of HCC cell lines. In addition, we proved that knockdown of PIK3R1 downregulated p-PI3K, p-AKT, and p-mTOR expressions in MHCC97H and HCCLM3 cells.ConclusionsIn conclusion, PIK3R1 providing potential novel targets for the treatment of HCC.

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“…Recent studies showed that breast cancer patients with higher miR‐107 concentrations have significantly lower probability of metastasis‐free survival 36,37 . On the other hand, miR‐502 has been shown to inhibit tumor cell proliferation in hepatocellular carcinoma in humans 38 …”

Section: Discussionmentioning

confidence: 99%

Extracellular vesicular microRNAs as potential biomarker for early detection of doxorubicin‐induced cardiotoxicity

Beaumier

Robinson

et al. 2020

Veterinary Internal Medicne

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Background: Long-term use of doxorubicin (DOX) is limited by cumulative dosedependent cardiotoxicity.Objectives: Identify plasma extracellular vesicle (EV)-associated microRNAs (miRNAs) as a biomarker for cardiotoxicity in dogs by correlating changes with cardiac troponin I (cTnI) concentrations and, echocardiographic and histologic findings.Animals: Prospective study of 9 client-owned dogs diagnosed with sarcoma and receiving DOX single-agent chemotherapy (total of 5 DOX treatments). Dogs with clinically relevant metastatic disease, preexisting heart disease, or breeds predisposed to cardiomyopathy were excluded.Methods: Serum concentration of cTnI was monitored before each treatment and 1 month after the treatment completion. Echocardiography was performed before treatments 1, 3, 5, and 1 month after completion. The EV-miRNA was isolated and sequenced before treatments 1 and 3, and 1 month after completion.Results: Linear mixed model analysis for repeated measurements was used to evaluate the effect of DOX. The miR-107 (P = .03) and miR-146a (P = .02) were significantly downregulated whereas miR-502 (P = .02) was upregulated. Changes in miR-502 were significant before administration of the third chemotherapeutic dose.When stratifying miRNA expression for change in left ventricular ejection fraction, upregulation of miR-181d was noted (P = .01). Serum concentration of cTnI changed significantly but only 1 month after treatment completion, and concentrations correlated with left ventricular ejection fraction and left ventricular internal dimension in diastole.Abbreviations: cTnI, cardiac troponin I; DOX, doxorubicin; E 0 , peak myocardial velocity in early diastole; ECG, electrocardiography; EV, extracellular vesicle; EV-miRNA, extracellular vesicle-associated miRNA; FAC, fractional area change; FS, fractional shortening; IVCT, isovolumic contraction time; IVRT, isovolumic relaxation time; LA:Ao, left atrium to aorta ratio; LVEF, left ventricular ejection fraction; LVIDdN, left ventricular end-diastolic internal diameter normalized to body weight; LVIDsN, left ventricular end-systolic internal diameter normalized to body weight; miRNAs, microRNAs; S 0 , peak myocardial velocity in systole.

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miR-502 inhibits cell proliferation and tumor growth in hepatocellular carcinoma through suppressing phosphoinositide 3-kinase catalytic subunit gamma

Cited by 22 publications

References 28 publications

CCND1, NOP14 and DNMT3B are involved in miR‐502‐5p–mediated inhibition of cell migration and proliferation in bladder cancer

CCND1, NOP14 and DNMT3B are involved in miR‐502‐5p–mediated inhibition of cell migration and proliferation in bladder cancer

Overexpression of PIK3R1 promotes hepatocellular carcinoma progression

Extracellular vesicular microRNAs as potential biomarker for early detection of doxorubicin‐induced cardiotoxicity

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