OBJECTIVEMicroRNA (miR)-93 has been proven to mediate the initiation and progression of colorectal carcinoma (CRC); however, the mechanisms by which miR-93 mediates CRC development need deeper elucidation. The present study is designed to investigate the association between miR-93 and high mobility group box 3 (HMGB3), as well as the functions of miR-93, in CRC.METHODSmiR-93 expression was quantified by RT-qPCR. CRC cells were transfected or cotransfected with miR-93 mimic, miR-93 inhibitor, pcDNA3.1-HMGB3 and sh-HMGB3, and then the proliferative, migratory and invasive capacities were detected in addition to the apoptotic rate. Western blotting assessed the expression levels of HMGB3, PI3K, p-PI3K, AKT and p-AKT. The interaction between miR-93 and HMGB3 was identified.RESULTSIn CRC tissues, miR-93 was downregulated and HMGB3 was upregulated. LOVO and SW480 cells transfected with miR-93 mimic exhibited reduced proliferation, invasion and migration as well as increased apoptosis. The ratios of p-PI3K/PI3K and p-AKT/AKT were declined after miR-93 mimic was introduced into the CRC cell lines. miR-93 negatively downregulated HMGB3, and introduction of pcDNA3,1-HMGB3 could counteract, in part, the inhibitory effects of miR-93 on the malignant properties of CRC cells as well as the ratios of p-PI3K/PI3K and p-AKT/AKT.CONCLUSIONmiR-93 targeted HMGB3 to block the activation of the PI3K/AKT pathway and thus enhance CRC cell apoptosis.

2019-02-01·Urologic Oncology: Seminars and Original Investigations3区 · 医学

MicroRNA-93 promotes bladder cancer proliferation and invasion by targeting PEDF

3区 · 医学

Article

作者: Wu, Aibin ; Jiang, Hua ; Bu, Qiang ; Zeng, Minghui ; Xia, Dongdong

OBJECTIVEMicroRNA-93 (miR-93) is upregulated in the urine of patients with bladder cancer (BC). Here, we investigated the role of miR-93 in BC progression and explored the underlying mechanism.METHODSmiR-93 expression in BC tissues and cells was detected by real time-polymerase chain reaction. The effects of miR-93 and pigment epithelium-derived factor (PEDF) on cell proliferation and invasion were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays. The binding of miR-93 to the 3'-untranslated region of PEDF was identified by the luciferase reporter assay.RESULTSmiR-93 expression was higher in BC tissues than in normal controls, and its expression was associated with tumor stage and node stage. Inhibition of miR-93 suppressed the proliferation and invasion of BC cells. PEDF was identified as a target of miR-93 and shown to mediate the effect of miR-93 on cell proliferation and invasion.CONCLUSIONSThe present data suggested that miR-93 promoted BC cell proliferation and invasion by targeting PEDF, providing new biomarkers and targets for BC diagnosis and treatment.

2017-12-01·European review for medical and pharmacological sciences

MiR-93 inhibition ameliorates OGD/R induced cardiomyocyte apoptosis by targeting Nrf2.

Article

作者: Fan, X-W ; Yan, L-J ; Yang, H-T ; Qiu, C-G ; Wu, J-T ; Wang, S-L

OBJECTIVETo identify the expression changes of microRNA 93 (miR-93) in oxygen-glucose deprivation/reoxygenation (OGD/R) injury in cardiomyocytes and its mechanism of mediating OGD/R and inducing apoptosis.MATERIALS AND METHODSPrimary cardiomyocytes were extracted and OGD/R model in cardiomyocytes was established in vitro. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expressions of miR-93, and Western blot assay was applied to measure the protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and caspase-3. Flow cytometry was utilized to examine the cardiomyocyte apoptosis rate.RESULTSThe apoptosis rate was increased after OGD/R in cardiomyocytes, accompanied by remarkable rise of miR-93 expression. After transfection of miR-93 antagomir, the apoptosis rate of cardiomyocyte induced by OGD/R was down-regulated, and the expression of cleaved caspase-3 was decreased. Meanwhile, the results of qRT-PCR and Western blot showed that the levels of Nrf2 mRNA and protein expression were up-regulated after the miR-93 level was inhibited, and luciferase reporter assay affirmed that Nrf2 was a target molecule for OGD/R-induced apoptosis mediated by miR-93.CONCLUSIONSmiR-93 mediates OGD/R-induced hypoxia/reoxygenation injury apoptosis in cells by targeting Nrf2.

100 项与 CPB-93 相关的药物交易

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