Search

Introduction: ABL2 contributes to the oncogenic potential of cancers, pointing to its inhibition as a possible strategy against malignant diseases. Bioinformatics prediction of upstream effector miR-30a-5p for ABL2 allowed us to hypothesize and then validate mechanistic actions of miR-30a-5p in lung adenocarcinoma (LUAD). Materials and methods: The ABL2 expression in LUAD was analyzed in the TCGA data, clinical samples, and cell lines. The shRNA-mediated silencing of ABL2 was introduced to illustrate its effect on malignant phenotypes of LUAD cells. The binding affinity between ABL2 and miR-30a-5p was verified by luciferase activity and RNA pull-down assay. Ectopic expression, knockdown methods, and PI3K inhibitor LY294002 were used to investigate their effects on in vitro biological characteristics and in vivo tumor growth of LUAD cells. Using nude mouse lung adenocarcinoma in situ and brain metastasis models to validate the inhibitory effect of miR-30a-5p on LUAD by regulating the ABL2/PI3K/AKT signaling axis. Results: High expression of ABL2 and poor expression of miR-30a-5p were noticed in LUAD tissues and cell lines. Importantly, miR-30a-5p was demonstrated to target and downregulate ABL2, subsequently inactivating the PI3K/AKT pathway. miR-30a-5p inhibited the malignant phenotypes of LUAD cells by inhibiting ABL2 expression and inactivating the PI3K/AKT pathway. For in vivo experiments, miR-30a-5p was substantiated to thwart tumor tumorigenesis by regulating the ABL2/PI3K/AKT axis. In addition, miR-30a-5p suppresses the occurrence and development of in situ lung cancer and brain metastasis via the ABL2/PI3K/AKT signaling pathway. Conclusion: This study underscores the inhibitory role of miR-30a-5p in LUAD through the ABL2/PI3K/AKT axis, which may be a viable target for LUAD treatment. [ABSTRACT FROM AUTHOR]

Objective: MicroRNA-30a-5p (miR-30a-5p) has been identified as a marker of heart failure; however, its functional mechanisms in chronic heart failure (CHF) remain unknown. We aim to investigate the role of miR-30a-5p targeting sirtuin-1 (SIRT1) in myocardial remodeling in CHF via the nuclear factor-κB/NOD-like receptor 3 (NF-κB/NLRP3) signaling pathway. Methods: CHF rat models were established using aortic coarctation. The expression of miR-30a-5p, SIRT1, and the NF-κB/NLRP3 signaling pathway-related factors in CHF rats was determined. The CHF rats were then respectively treated with altered miR-30a-5p or SIRT1 to explore their roles in cardiac function, myocardial function, inflammatory response, pathological changes, and cardiomyocyte apoptosis. The binding relation between miR-30a-5p and SIRT1 was confirmed. Results: MiR-30a-5p was upregulated whereas SIRT1 was downregulated in myocardial tissues of CHF rats. MiR-30a-5p inhibition or SIRT1 overexpression improved cardiac and myocardial function, and suppressed the inflammatory response, alleviated pathological changes and inhibited cardiomyocyte apoptosis in CHF rats. MiR-30a-5p targeted SIRT1 to regulate the NF-κB/NLRP3 signaling pathway. In CHF rats, downregulated miR-30a-5p and silenced SIRT1 could reverse the beneficial effects of downregulated miR-30a-5p. Conclusion: Inhibited miR-30a-5p inhibits CHF progression via the SIRT1-mediated NF-κB/NLRP3 signaling pathway. [ABSTRACT FROM AUTHOR]

LINC00488 confers oncogenic activity in the progression of some tumors. Hence, the target of the study was about to specify LINC00488-mediated network in retinoblastoma (RB). LINC00488 expression was tested in RB clinical tissues. siRNA targeting LINC00488 or miR-30a-5p mimic was introduced into RB cell line (Y79) to observe cellular biological functions. The relationship between LINC00488, miR-30a-5p and EPHB2 was verified. Afterward, the role of miR-30a-5p involved in RB through targeted regulation of EPHB2 was probed in vitro and in vivo. LINC00488 was induced in RB tissue and cells. LINC00488 knockdown or miR-30a-5p upregulation depressed the malignant activities of Y79 cells. LINC00488 could sponge miR-30a-5p that targeted EPHB2. EPHB2, and EPHB2 overexpression counteracted miR-30a-5p restoration-induced inhibition of Y79 cell development in vitro and in vivo. LINC00488 induces tumorigenicity in RB by binding to miR-30a-5p to target EPHB2, which may offer a new clue of RB treatment from an lncRNA–miRNA–mRNA network. [ABSTRACT FROM AUTHOR]

Abstract Background The development of morphine tolerance is a clinical challenge for managing severe pain. Studies have shown that neuroinflammation is a critical aspect for the development of analgesic tolerance. We found that AMPK-autophagy activation could suppress neuroinflammation and improve morphine tolerance via the upregulation of suppressor of cytokine signaling 3 (SOCS3) by inhibiting the processing and maturation of microRNA-30a-5p. Methods CD-1 mice were utilized for the tail-flick test to evaluate morphine tolerance. The microglial cell line BV-2 was utilized to investigate the mechanism of AMPK-autophagy-mediated posttranscriptional regulation of SOCS3. Proinflammatory cytokines were measured by western blotting and real-time PCR. The levels of SOCS3 and miRNA-processing enzymes were evaluated by western blotting, real-time PCR and immunofluorescence staining. Results Based on experimental verification, miRNA-30a-5p could negatively regulate SOCS3. The AMPK activators AICAR, resveratrol and metformin downregulated miRNA-30a-5p. We found that AMPK activators specifically inhibited the processing and maturation of miRNA-30a-5p in microglia by degrading DICER and AGO2 via autophagy. Furthermore, a miRNA-30a-5p inhibitor significantly improved morphine tolerance via upregulation of SCOS3 in mice. It markedly increased the level of SOCS3 in the spinal cord of mice and subsequently inhibited morphine-induced phosphorylation of NF-κB p65. In addition, a miRNA-30a-5p inhibitor decreased the levels of IL-1β and TNF-α caused by morphine in microglia. Conclusion AMPK-autophagy activation suppresses neuroinflammation and improves morphine tolerance via the upregulation of SOCS3 by inhibiting miRNA-30a-5p.

Purpose: To determine the effect of miR-30a-5p on hepatoma cell radiosensitivity and elucidate the underlying mechanism. Methods: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to measure miR-30a-5p expression in HepG2 and THLE-3 cells. After 4-Gy X-ray irradiation or miR-30a-5p mimic transfection, the miR-30a-5p level in HepG2 cells was determined using qRT-PCR. Luciferase reporter assay was used to confirm the correlation between miR-30a-5p and glucose-regulated protein 78 (GRP78) levels, while the effects of miR-30a-5p on the viability of HepG2 cells were determined using clone formation and 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assays. Apoptotic cells were evaluated by flow cytometry whereas the protein levels of GRP78, B-cell lymphoma-2 (Bcl-2), BCL2-Associated X Protein (Bax), and cleaved-caspase-9 were quantified by immunoblotting. Results: MicroRNA-30a-5p expression was decreased in HepG2 cells but reduced after 4-Gy x-ray treatment, while miR-30a-5p mimic transfection upregulated miR-30a-5p expression (p < 0.05). Cell viability was inhibited after x-ray irradiation or miR-30a-5p mimic transfection and further inhibited by irradiation + miR-30a-5p (p < 0.05). Irradiation or miR-30a-5p transfection triggered cell apoptosis; however, irradiation + miR-30a-5p induced more apoptosis, upregulated Bax and cleaved-caspase-9 expression, and reduced Bcl-2 expression (p < 0.05). MicroRNA-30a-5p also suppressed GRP78 expression. Conclusion: MicroRNA-30a-5p may enhance HCC x-ray radiosensitivity by inhibiting GRP78., and may be useful in developing treatment strategies for HCC patients. [ABSTRACT FROM AUTHOR]

Long noncoding RNA HOX transcript antisense RNA (HOTAIR) has been studied in multiple diseases, but the role of HOTAIR on chronic heart failure (CHF) through the regulation of microRNA (miR)‐30a‐5p and lysine‐specific demethylase 3A (KDM3A) remains unexplored. This research aims to probe the effects of HOTAIR on CHF progression via modulating miR‐30a‐5p to target KDM3A. CHF mouse model was established by intraperitoneal injection of doxorubicin. The CHF mice were then injected with high‐expressed HOTAIR, miR‐30a‐5p or KDM3A adenovirus vectors to determine the cardiac function, oxidative stress, inflammatory response, pathological change and cardiomyocyte apoptosis. HOTAIR, miR‐30a‐5p, KDM3A and Bcl‐2/adenovirus E1B 19kDa interacting protein 3 (BNIP3) expression in CHF mice was detected. The binding relations among HOTAIR, miR‐30a‐5p and KDM3A were validated. HOTAIR and KDM3A were depleted, while miR‐30a‐5p was augmented in CHF mice. The elevated HOTAIR or KDM3A or could improve cardiac function, mitigate oxidative stress and pathological change, reduce inflammatory factor levels and cardiomyocyte apoptosis, while the increased miR‐30a‐5p exerted opposite effects. The miR‐30a‐5p elevation could reverse the effects of enriched HOTAIR, while BNIP3 reduction abrogated the effects of KDM3A on CHF. HOTAIR sponged miR‐30a‐5p that targeted KDM3A. HOTAIR improves cardiac injury in CHF via modulating miR‐30a‐5p to target KDM3A. This study provides novel therapeutic strategies for CHF treatment. [ABSTRACT FROM AUTHOR]

Background: The development of morphine tolerance is a clinical challenge for managing severe pain. Studies have shown that neuroinflammation is a critical aspect for the development of analgesic tolerance. We found that AMPK-autophagy activation could suppress neuroinflammation and improve morphine tolerance via the upregulation of suppressor of cytokine signaling 3 (SOCS3) by inhibiting the processing and maturation of microRNA-30a-5p.Methods: CD-1 mice were utilized for the tail-flick test to evaluate morphine tolerance. The microglial cell line BV-2 was utilized to investigate the mechanism of AMPK-autophagy-mediated posttranscriptional regulation of SOCS3. Proinflammatory cytokines were measured by western blotting and real-time PCR. The levels of SOCS3 and miRNA-processing enzymes were evaluated by western blotting, real-time PCR and immunofluorescence staining.Results: Based on experimental verification, miRNA-30a-5p could negatively regulate SOCS3. The AMPK activators AICAR, resveratrol and metformin downregulated miRNA-30a-5p. We found that AMPK activators specifically inhibited the processing and maturation of miRNA-30a-5p in microglia by degrading DICER and AGO2 via autophagy. Furthermore, a miRNA-30a-5p inhibitor significantly improved morphine tolerance via upregulation of SCOS3 in mice. It markedly increased the level of SOCS3 in the spinal cord of mice and subsequently inhibited morphine-induced phosphorylation of NF-κB p65. In addition, a miRNA-30a-5p inhibitor decreased the levels of IL-1β and TNF-α caused by morphine in microglia.Conclusion: AMPK-autophagy activation suppresses neuroinflammation and improves morphine tolerance via the upregulation of SOCS3 by inhibiting miRNA-30a-5p. [ABSTRACT FROM AUTHOR]

Viral myocarditis (VMC) is a life-threatening disease characterized by severe cardiac inflammation generally caused by coxsackievirus B3 (CVB3) infection. Several microRNAs (miRNAs or miRs) are known to play crucial roles in the pathogenesis of VMC. The study aimed to decipher the role of miR-30a-5p in the underlying mechanisms of VMC pathogenesis. We first quantified miR-30a-5p expression in a CVB3-induced mouse VMC model. The physiological characteristics of mouse cardiac tissues were then detected by hematoxylin and eosin (HE) and Picrosirius red staining. We established the correlation between miR-30a-5p and SOCS1, using dual-luciferase gene assay and Pearson's correlation coefficient. The expression of inflammatory factors (IFN-γ, IL-6, IL-10, and IL-13), M1 polarization markers [TNF-α, inducible nitric oxide synthase (iNOS)], M2 polarization markers (Arg-1, IL-10), and myocardial hypertrophy markers [atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)] was detected by RT-qPCR and Western blot analysis. miR-30a-5p was found to be highly expressed in VMC mice. Silencing of miR-30a-5p improved the cardiac function index and reduced heart weight-to-body weight ratio, myocardial tissue pathological changes and fibrosis degree, serological indexes, as well as proinflammatory factor levels, while enhancing anti-inflammatory factor levels in VMC mice. Furthermore, silencing of miR-30a-5p inhibited M1 polarization of macrophages while promoting M2 polarization in vivo and in vitro. SOCS1 was a target gene of miR-30a-5p, and the aforementioned cardioprotective effects of miR-30a-5p silencing were reversed upon silencing of SOCS1. Overall, this study shows that silencing of miR-30a-5p may promote M2 polarization of macrophages and improve cardiac injury following VMC via SOCS1 upregulation, constituting a potential therapeutic target for VMC treatment. [ABSTRACT FROM AUTHOR]

Exosomes carrying microRNAs (miRNAs) have been demonstrated to play critical roles in the regulation of development, growth and metastasis of cancer. Bioinformatic predictions identified differentially expressed SRY-box 9 (SOX9) in OC, and the regulatory miRNA miR-139-5p. Here, we aim to evaluate the function of exosomal miR-139-5p in the sensitivity of ovarian cancer (OC) cells to cis-diamminedichloroplatinum(II) (DDP). Expression pattern of miR-139-5p and SOX9 in ovarian cancer cells (SKOV3) and DDP-resistant cells (SKOV3/DDP) was identified using reverse transcription quantitative polymerase chain reaction and western blot analysis. The relationship between miR-139-5p and SOX9 was validated using a dual-luciferase reporter assay. SKOV3/DDP cell line was developed and introduced with miR-30a-5p mimic to analyse the effects of miR-30a-5p on resistance to DDP. The in vitro and in vivo effects of exosomal miR-30a-5p on resistance of SKOV3 cells to DDP were assessed in a co-culture system of exosomes and OC cells as well as in tumour-bearing nude mice. High expression of SOX9 and low expression of miR-30-5p were witnessed in OC. Furthermore, miR-30-5p, a downregulated miRNA in SKOV3/DDP cells, increased the rate of cell apoptosis and enhanced the sensitivity of SKOV3/DDP cells to DDP by targeting SOX9. Moreover, exosomes carrying miR-30a-5p were identified to sensitize SKOV3/DDP cells to DDP both in vitro and in vivo. These data together supported an important conclusion that DDP-resistant OC cell-derived exosomal miR-30a-5p enhanced cellular sensitivity to DDP, highlighting a potential strategy to overcome drug resistance.

Nowadays, many studies focus on the relationship between microRNAs (miRs) and the development of oral squamous cell carcinoma (OSCC). Here, we broaden the understanding of miR-30a-5p in OSCC. In silico analysis was implemented to screen differentially expressed genes in OSCC and the related upstream regulatory miR. OSCC SCC9 cells were manipulated with lentivirus-mediated miR-30a-5p mimic, oe-ITGA6 or sh-ITGA6 and LY294002 (the PI3K/AKT pathway inhibitor) for studying their roles in cell biological processes. Tumors were xenografted in nude mouse for in vivo mechanism verification. In silico analysis results depicted that ITGA6 was highly expressed in OSCC, and that miR-30a-5p was the upstream regulatory miR of ITGA6. miR-30a-5p was downregulated and ITGA6 was highly expressed in OSCC tissues and cells. miR-30a-5p targeted and downregulated ITGA6. ITGA6 promoted epithelial-mesenchymal transition, migration and invasion in OSCC cells by activating PI3K/AKT pathway. miR-30a-5p could suppress the in vivo growth and metastasis of OSCC by inhibiting the ITGA6/PI3K/AKT axis. Taken together, miR-30a-5p prevents OSCC progression by inhibiting PI3K/AKT pathway through inhibition of ITGA6 expression. [ABSTRACT FROM AUTHOR]

Background/Aims: MiR-30a-5p, a member of the microRNA-30 family (miR-30), is known to function as a tumor suppressor in several different cancers. However, the expression levels, biological function, and underlying mechanisms of miR-30a-5p in renal cell carcinoma (RCC) remain unclear. Glucose-regulated protein78 (GRP78) is a common cancer biomarker and promotes the growth and survival of cancer cells. The expression of GRP78 has been reported to be modulated by miR-30a in neurons. In this study, the expression profile of miR-30a-5p in clear cell renal cell carcinoma (ccRCC) and its effect on ccRCC through regulating GRP78 expression was investigated. Methods: MiR-30a-5p expression was analyzed using bioinformatic software on open microarray datasets from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), and confirmed by quantitative RT-PCR (qRT-PCR) in ccRCC cell lines. Cell proliferation was investigated using CCK-8 and cell count assays. Western blotting, immunohistochemistry, luciferase reporter assays, and flow cytometry were employed to investigate the mechanisms of the effect of miR-30a-5p on ccRCC Results: MiR-30a-5p was down-regulated in ccRCC and related to the clinicopathological factors and prognosis of ccRCC. MiR-30a-5p was found to both suppress the growth of ccRCC cells and promote apoptosis of ccRCC cells in vitro. GRP78 was the direct target gene of miR-30a-5p, and the GRP78 expression was inversely correlated with the expression of miR-30a-5p in vivo and in vitro. The functional studies of GRP78 overexpression or knockdown demonstrated that GRP78 promoted proliferation and anti-apoptosis of ccRCC cells, and the oncogenic activity of GRP78 resulting in by miR-30a-5p overexpression. Conclusion: MiR-30a-5p is a bona fide negative regulator of GRP78 expression, and the anti-tumor activity of miR-30a-5p in ccRCC is due at least in part to down-regulating GRP78 expression and modulating the unfolded protein response (UPR) pathway. Thus, miR-30-GRP78 interaction provides a novel therapeutic candidate target in ccRCC treatment.

Pulmonary arterial hypertension (PAH) is a fatal and currently incurable cardiopulmonary disease. Numerous microRNAs (miRNAs) serve important roles in the development of PAH. While the expression of miR-30a-5p was downregulated in the lung tissue of rats in a pulmonary hypertension rat model, the expression pattern and function of miR-30a-5p in human PAH remain unclear. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to examine miR-30a-5p and chitinase-3-like protein 1 (YKL-40) mRNA expression levels. The expression levels of YKL-40 and apoptosis-associated proteins were measured by western blot analysis. Cell proliferation assays and flow cytometry analysis were performed to examine cell proliferation and apoptosis, respectively. The association between miR-30a-5p and YKL-40 was determined by a luciferase reporter assay, RT-qPCR and western blot analysis. The relative expression levels of miR-30a-5p in plasma were increased in patients with PAH [median=13.23 (25th percentile=6.388, 75th percentile=21.91)] compared with normal controls [median=2.25 (25th percentile=1.4, 75th percentile=3.7). The expression of miR-30a-5p was significantly downregulated while the protein expression of YKL-40 was significantly upregulated in hypoxia-induced human pulmonary artery endothelial cells (HPAECs) when compared with the hypoxia-induced group at 0 h. miR-30a-5p overexpression promoted HPAEC growth and inhibited apoptosis of HPAECs under hypoxia. A miR-30a-5p mimic decreased the luciferase activity of a luciferase reporter construct containing YKL-40 3′-untranslated region and also decreased YKL-40 protein expression. YKL-40 overexpression partly alleviated the effects of miR-30a-5p upregulation on proliferation and apoptosis of HPAECs under hypoxia. In conclusion, the data indicated that miR-30a-5p promoted cell growth and inhibited apoptosis of HPAECs under hypoxia by targeting YKL-40. Therefore, the miR-30a-5p/YKL-40 axis may provide a potential target for the development of novel PAH therapies. [ABSTRACT FROM AUTHOR]

Keloids are benign fibrous overgrowths that occur as a result of abnormal wound healing following cutaneous injury. MicroRNAs (miRNAs/miRs) are short non-coding RNAs that serve critical roles in numerous important biological processes, such as cell proliferation, differentiation and apoptosis. However, their role in keloid development remains largely unknown. In the present study, the role of miR-30a-5p, a miRNA regulated by Trichostatin A (TSA), in apoptosis within cultured keloid fibroblasts was investigated. An MTT assay was used to detect the proliferation of cultured keloid fibroblasts treated with TSA. Cell apoptosis and cell cycle phases were analyzed using flow cytometry. In addition, an miRNA microarray was performed to compare expression profiles between cultured keloid fibroblasts treated with or without 1,000 nM TSA. Reverse transcription-quantitative polymerase chain reaction analysis was conducted to estimate miRNA expression levels. The direct target of miR-30a-5p was identified using a dual-luciferase reporter assay. Western blotting was employed to assess protein expression levels in keloid fibroblasts. The results demonstrated that TSA inhibited the proliferation of keloid fibroblasts in a time- and dose-dependent manner. The miRNA microarray revealed alterations in the expression of numerous miRNA sequences in response to TSA when compared with controls. Notably, the expression of miR-30a-5p was downregulated in keloid tissues. In addition, overexpression of miR-30a-5p induced apoptosis by targeting B-cell lymphoma 2, which was similar to that observed in response to TSA. These results provide important information regarding a novel miR-30a-5p-mediated signaling pathway induced by TSA treatment, and suggest a potential use for TSA and miR-30a-5p as effective therapeutic strategies for keloids. [ABSTRACT FROM AUTHOR]

MicroRNA (miR)‑30a‑5p has been reported to suppress the progression of hepatocellular cancer, renal cell carcinoma, oral cancer and gastric cancer. However, whether miR‑30a‑5p is involved in the regulation of melanoma remains unclear. The present study revealed that miR‑30a‑5p was downregulated in melanoma tissues and cell lines. Overexpression of miR‑30a‑5p significantly inhibited the proliferation, migration and invasion of melanoma cells in vitro. In addition, ectopic expression of miR‑30a‑5p delayed tumor growth in vivo. In terms of mechanism, miR‑30a‑5p targeted sex determining region Y‑box 4 (SOX4) and impeded the expression of SOX4 in melanoma cells. In addition, SOX4 was upregulated in melanoma tissues and cell lines when compared with normal tissues or cells. Furthermore, overexpression of SOX4 significantly rescued the proliferation, migration and invasion of melanoma cells transfected with miR‑30a‑5p mimics. Taken together, the results of the present study demonstrated that miR‑30a‑5p suppressed the proliferation, migration and invasion of melanoma cells in SOX4‑dependent manner. [ABSTRACT FROM AUTHOR]

Cypermethrin (CYP) has been identified as one kind of endocrine-disrupting chemicals (EDCs) to induce male reproduction damage. This study aimed to investigate the effects and mechanisms of miR-30a-5p on CYP induced apoptosis of TM4 mouse Sertoli cells in vitro. In the present study, 0 μM, 10 μM, 20 μM, 40 μM and 80 μM CYP were used to treat TM4 cells for 24 h. The apoptosis of TM4 cells, the expression level of miR-30a-5p, the protein expressions and the interaction between miR-30a-5p and KLF9 were detected by flow cytometry, quantitative Real-Time PCR, Western blot and luciferase reporter assays. CYP induced apoptosis of TM4 cells, inhibited expression of miR-30a-5p in TM4 cells, and overexpression of miR-30a-5p partially recovered CYP induced cells apoptosis. Furthermore, KLF9 was a potential downstream target of miR-30a-5p predicted by publicly available databases. KLF9 expression level in TM4 cells was significantly elevated after treatment with CYP, and the induction was inhibited by miR-30a-5p mimics transfection. Meanwhile, dual-luciferase reporter assay demonstrated that miR-30a-5p directly targeted KLF9–3′UTR. Moreover, in the presence of CYP, the apoptosis regulator p53 expression was also increased in TM4 cells. Overexpression miR-30a-5p or down-regulation of KLF9 both attenuated the induction of CYP on p53 expression. Overall, the present study demonstrated that miR-30a-5p regulated CYP induced TM4 cells apoptosis by targeting KLF9/p53 axis. • miR-30a-5p regulated cypermethrin-induced apoptosis of TM4 cells. • KLF9 was a downstream target of miR-30a-5p. • miR-30a-5p regulated TM4 cells apoptosis by targeting KLF9/p53 axis. [ABSTRACT FROM AUTHOR]

Background/Aims: MiR-30a-5p, a member of the microRNA-30 family (miR-30), is known to function as a tumor suppressor in several different cancers. However, the expression levels, biological function, and underlying mechanisms of miR-30a-5p in renal cell carcinoma (RCC) remain unclear. Glucose-regulated protein78 (GRP78) is a common cancer biomarker and promotes the growth and survival of cancer cells. The expression of GRP78 has been reported to be modulated by miR-30a in neurons. In this study, the expression profile of miR-30a-5p in clear cell renal cell carcinoma (ccRCC) and its effect on ccRCC through regulating GRP78 expression was investigated. Methods: MiR-30a-5p expression was analyzed using bioinformatic software on open microarray datasets from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), and confirmed by quantitative RT-PCR (qRT-PCR) in ccRCC cell lines. Cell proliferation was investigated using CCK-8 and cell count assays. Western blotting, immunohistochemistry, luciferase reporter assays, and flow cytometry were employed to investigate the mechanisms of the effect of miR-30a-5p on ccRCC. Results: MiR-30a-5p was down-regulated in ccRCC and related to the clinicopathological factors and prognosis of ccRCC. MiR-30a-5p was found to both suppress the growth of ccRCC cells and promote apoptosis of ccRCC cells in vitro. GRP78 was the direct target gene of miR-30a-5p, and the GRP78 expression was inversely correlated with the expression of miR-30a-5p in vivo and in vitro. The functional studies of GRP78 overexpression or knockdown demonstrated that GRP78 promoted proliferation and anti-apoptosis of ccRCC cells, and the oncogenic activity of GRP78 resulting in by miR-30a-5p overexpression. Conclusion: MiR-30a-5p is a bona fide negative regulator of GRP78 expression, and the anti-tumor activity of miR-30a-5p in ccRCC is due at least in part to down-regulating GRP78 expression and modulating the unfolded protein response (UPR) pathway. Thus, miR-30-GRP78 interaction provides a novel therapeutic candidate target in ccRCC treatment. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRs) are a class of small non-coding RNAs of 18-25 nucleotides in length that serve as key regulators in the development and progression of human cancers. Recently, miR-30b-5p, as a member of the miR-30 family, has been reported to act as a tumor suppressor in gastric cancer. However, the expression and function of miR-30a-5p in gastric cancer, as well as the corresponding underlying mechanism, remain unknown. In the present study, it was demonstrated that the expression of miR-30a-5p was significantly reduced in gastric cancer tissues (n=43) compared with normal gastric tissues (n=10; P<0.01). Similarly, miR-30a-5p was significantly downregulated in the gastric cancer cell lines AGS, HGC27, BGC823 and SGC7901, when compared with the normal gastric mucosa epithelial cell line GES-1 (P<0.01). In addition, overexpression of miR-30a-5p significantly inhibited the proliferation and invasion of AGS cells (P<0.01). Insulin-like growth factor 1 receptor (IGF-1R) was identified as a novel target of miR-30a-5p, and the protein expression of IGF-1R was negatively regulated by miR-30a-5p in AGS cells (P<0.01). Furthermore, overexpression of IGF-1R significantly reversed the inhibitory effect of miR-30a-5p on the proliferation and invasion of AGS cells (P<0.01), indicating that IGF-1R was involved in miR-30a-5p-mediated proliferation and invasion of AGS cells. It was also observed that the expression of IGF-1R mRNA was upregulated in gastric cancer tissues compared with normal gastric tissues (P<0.01), and its levels of expression were reversely correlated with that of miR-30a-5p in gastric cancer tissues (R²=0.3892; P<0.01). Collectively, these data suggest that miR-30a-5p inhibits the growth and metastasis of gastric cancer by directly targeting IGF-1R. Therefore, the miR-30a-5p/IGF-1R axis may be a potential therapeutic target in the treatment of gastric cancer. [ABSTRACT FROM AUTHOR]

Accumulating studies reported mutations in the gene encoding the proline-rich transmembrane protein 2 (PRRT2) to be causative for several paroxysmal neurological disorders, including paroxysmal kinesigenic dyskinesia (PKD), PKD combined with infantile seizures (ICCA), and benign familial infantile seizures (BFIS). However, the impact of PRRT2 in tumorigenesis is not known. Based on a large-scale data analysis, we found that PRRT2 was down-regulated in glioma tumor tissues compared with normal brain tissue. Dysregulation of PRRT2 was not induced by mutation, copy number variation and epigenetic modification, but modulated by microRNA-30a-5p. Overexpression of PRRT2 strongly impaired the cell viability and promoted cell apoptosis and these anti-tumor effects could be largely reversed by microRNA-30a-5p. Mechanistically, PRRT2 expression was closely correlated genes involved in unfolded protein response (UPR) pathway and introduction of PRRT2 inhibited gene expression in the three branches of UPR, including PERK axis, IRE1 axis and ATF6 axis. Taken together, our findings identify PRRT2 as a tumor suppressor in glioma and provide a promising target for potential therapeutic intervention. [ABSTRACT FROM AUTHOR]

• circ_0002612 upregulates PPARGC1A by competitively binding to miR-30a-5p. • circ_0002612 induces cardiomyocyte proliferation via the miR-30a-5p/PPARGC1A axis. • PPARGC1A reduces NLRP3 expression to augment cardiomyocyte proliferation. • circ_0002612 alleviates MIRI by inhibiting the expression of NLRP3. • This study offers a novel mechanistic understanding and therapeutic target for MIRI. Novel mechanistic insights into the effects of circular RNAs (circRNAs) on the physiology and pathology of cardiovascular diseases are under increasingly active investigation. This study defined the cardioprotective role and mechanistic actions of circ_0002612 in myocardial ischemia/reperfusion injury (MI/RI). MI/RI was induced in mice by ligation of the left anterior descending (LAD) artery followed by reperfusion, and the in vitro model was established in cultured cardiomyocytes under hypoxia/reoxygenation (H/R) conditions. Interaction among circ_0002612, miR-30a-5p, Ppargc1a, and NLRP3 was predicted by bioinformatics analysis and further experimentally identified. Gain- and loss-of-function experiments were performed to evaluate the effect of the circ_0002612/miR-30a-5p/Ppargc1a/NLRP3 axis on the cardiac function and myocardial infarction of I/R-injured mice, as well as viability and apoptosis of H/R-challenged cardiomyocytes. In the myocardial tissues of MI/RI mice, miR-30a-5p was negatively correlated with circ_0002612 or Ppargc1a, but circ_0002612 was positively correlated with the expression of Ppargc1a. circ_0002612 competitively bound to miR-30a-5p to release expression of its target gene Ppargc1a. circ_0002612 promoted cardiomyocyte viability while suppressing the apoptosis by impairing the miR-30a-5p-mediated inhibition of Ppargc1a. Additionally, Ppargc1a inhibited the expression of NLRP3 and consequently facilitated cardiomyocyte proliferation while suppressing cell apoptosis. By inhibiting the expression of NLRP3, circ_0002612 protected mice from MI/RI. Overall, this study demonstrates the cardioprotective role of circ_0002612 against MI/RI, which may be a viable target for MI/RI. [ABSTRACT FROM AUTHOR]

The present study aimed to explore the expression of microRNA (miRNA or miR) in drug-resistant and drug-sensitive ovarian cancer cell lines, and to seek the potential therapeutic target of ovarian cancer drug-resistant mechanism in order to improve drug resistance by altering miRNA levels. The drug-resistant characteristics of SKOV3/DDP, SKOV3, COC1/DDP and COC1 cell lines were studied. The miRNAs that were differentially expressed between cisplatin-resistant cells and its parental cells in ovarian cancer were screened with a miRNA chip. The effect of miRNAs was detected, and their drug-resistant mechanism was investigated by transfection and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide methods. Among the expression screening of miRNAs, 41 mRNAs, including Homo sapiens (hsa)-miR-30a-5p and hsa-miR-34c-5p, were highly expressed in the drug-resistant cells, whereas 44 miRNAs, including hsa-miR-96-5p and hsa-miR-200c-3p, were lowly expressed. The expression levels of hsa-miR-30a-5p in two types of ovarian cancer chemotherapy-resistant cell lines were significantly higher than those in chemotherapy-sensitive cell lines, which was associated with ovarian cancer chemotherapy resistance. In conclusion, high expression of miRNA-30a-5p was able to promote cell growth and colony forming ability, and enhance cell migration and invasion. Thus, miRNA-30a-5p is expected to become a meaningful novel target for ovarian cancer resistant treatment. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma (RCC) is the most common type of malignant tumor of the adult kidney and has a poor prognosis. MicroRNAs (miRs) are important in a wide range of biological and pathological processes, including cell differentiation, migration, growth, proliferation, apoptosis and metabolism. The present study aimed to determine the role exerted by miR-30a-5p in the tumorigenesis of RCC. The expression levels of miR-30a-5p in RCC tissues and RCC-derived cells were demonstrated to be significantly downregulated by real-time quantitative polymerase chain reaction (RT-qPCR). Wound scratch assay, cell proliferation assay and flow cytometric analysis revealed that the abilities of migration and proliferation of the RCC-derived cells were suppressed, whereas cell apoptosis was promoted, when miR-30a-5p was overexpressed in these cells. N-acetylgalactos aminyltransferase 7 (GALNT7) was predicted to be one target gene of miR-30a-5p by bioinformatics analysis. Luciferase reporter assay, RT-qPCR and western blotting were performed to confirm that GALNT7 is the direct conserved target of miR-30a-5p. These results suggested that miR-30a-5p has a tumor-suppressive role in the tumorigenesis of RCC. [ABSTRACT FROM AUTHOR]

Objective: The aim of the study was to investigate the role of miR-30a-5p in restenosis of rats following vein grafting and the underlying mechanism., Methods: Vein graft rat models were established and perfused with miR-30a-5p antagomir and si-ATG5 to probe the regulation of miR-30a-5p/ATG5 on intimal hyperplasia. Human saphenous vein smooth muscle cells (HSVSMCs) were obtained from the great saphenous veins of patients undergoing coronary artery bypass grafting and subjected to assays for autophagy, proliferation, and migration after gain and loss of function of miR-30a-5p and/or ATG5. The binding of miR-30a-5p and ATG5 was confirmed by RIP and dual-luciferase reporter assays., Results: MiR-30a-5p expression gradually increased, ATG5 expression gradually decreased, and the intima was increasingly thickened during restenosis of grafted veins. Knockdown of miR-30a-5p in rats repressed the restenosis of vein grafts, while a deficiency of ATG5 reversed the effect of miR-30a-5p inhibition. Upregulation of miR-30a-5p enhanced the proliferation and migration of HSVSMCs and inhibited the autophagy, while downregulation of miR-30a-5p or overexpression of ATG5 showed opposite effects. ATG5 is a target gene of miR-30a-5p., Conclusion: MiR-30a-5p exacerbates vein graft restenosis by repressing ATG5 expression and inhibiting autophagy., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Acute kidney injury (AKI) is a susceptible factor for chronic kidney disease (CKD). There is still a lack of effective prevention methods in clinical practice. This study investigated the protective effect of the urinary exosomes from premature infants on cisplatin-induced acute kidney injury. Here we isolated exosomes from the fresh urine of premature infants. A C57BL/6 mice model of cisplatin-induced acute kidney injury was given 100 ug urinary exosomes 24 hours after model establishment. The kidneys were collected for pathological examination and the evaluation of renal tubular damage and apoptosis. In the in vitro experiment, human renal cortex/proximal tubular cells (HK-2) were induced by cisplatin to assess the effect of the urine exosomes from premature infants. Exosome microRNA (miRNA) sequencing technology was applied to investigate the miRNAs enriched in exosomes and the dual-luciferase gene reporter system to examine the targeting relationship of the miRNA with target genes. The results indicated that the urinary exosomes could decrease the serum creatinine level and the apoptosis of renal tubular cells, and reduce mice mortality. In addition, miR-30a-5p was the most abundant miRNA in the exosomes. It protected HK-2 cells from cisplatin-induced apoptosis by targeting and down-regulating the mitogen-activated protein kinase 8 (MAPK8). Together, our findings identified that the urinary exosomes derived from premature infants alleviated cisplatin-induced acute kidney injury and inhibited the apoptosis of HK-2 via miR-30a-5p, which could target MAPK8. These findings implied that urinary exosomes from premature infants riched in miR-30a-5p might become a potential treatment for AKI.

Curcumin has been shown to inhibit the growth of a variety of tumor cells. However, the biological functions of curcumin in prostate cancer (PCa) have not yet fully elucidated. The objective of the present study was to investigate the role of curcumin on the proliferation, migration, invasion and apoptosis of PCa cells and the underlying mechanism. Cell Counting Kit-8 and flow cytometry were used to detect the effects of curcumin at different concentrations on the proliferation and apoptosis of PCa cell lines, PC-3 and DU145. BrdU and Transwell assays, western blotting and reverse transcription-quantitative PCR were used to determine the effect of curcumin on cell proliferation, migration and invasion, apoptosis-related protein expression, and microRNA (miR)-30a-5p and PCNA clamp associated factor (PCLAF) expression, respectively. In addition, bioinformatics analysis and Pearson's correlation test were used to verify the relationship between miR-30a-5p and PCLAF. Curcumin was observed to impede the proliferation, migration and invasion of PCa cells, and promote their apoptosis in a time- and dose-dependent manner. Curcumin enhanced miR-30a-5p expression and inhibited PCLAF expression; furthermore, there was a negative correlation between miR-30a-5p and PCLAF expression in PCa tissues. In addition, transfection of miR-30a-5p inhibitors partially reversed the function of curcumin on cell proliferation, migration, invasion and apoptosis. Overall, curcumin suppressed the malignant biological behaviors of PCa cells by regulating the miR-30a-5p/PCLAF axis. [ABSTRACT FROM AUTHOR]

Our previous study reported that microRNA (miR)-30a-5p upregulation under hypoxia postconditioning (HPostC) exert a protective effect on aged H9C2 cells against hypoxia/reoxygenation injury via DNA methyltransferase 3B-induced DNA hypomethylation at the miR-30a-5p gene promoter. This suggests that miR-30a-5p may be a potential preventative and therapeutic target for ischemic heart disease in aged myocardium. The present study aimed to investigate the underlying mechanisms of miR-30a-5p transcription in aged myocardium in ischemic heart disease. Cardiomyocytes were treated with 8 mg/ml D-galactose for 9 days, and then exposed to hypoxic conditions. Cell viability was determined using a cell viability assay. Expression levels of histone deacetylase 2 (HDAC2), LC3B-II/I, beclin-1 and p62 were detected via reverse transcription-quantitative PCR and western blotting. Chromatin immunoprecipitation-PCR and luciferase reporter assays were performed to evaluate the effect of c-Myc binding and activity on the miR-30a-5p promoter in senescent cardiomyocytes following HPostC. It was found that HPostC enhanced the acetylation levels of H3K14 at the miR-30a-5p gene promoter in senescent cardiomyocytes, which attributed to the decreased expression of HDAC2. In addition, c-Myc could positively regulate miR-30a-5p transcription to inhibit senescent cardiomyocyte autophagy. Mechanically, it was observed that increased H3K14 acetylation level exposed to romidepsin facilitated c-Myc binding to the miR-30a-5p gene promoter region, which led to the increased transcription of miR-30a-5p. Taken together, these results demonstrated that HDAC2-mediated H3K14 hyperacetylation promoted c-Myc binding to the miR-30a-5p gene promoter, which contributed to HPostC senescent cardioprotection. [ABSTRACT FROM AUTHOR]

MicroRNA-30a-5p (miR-30a-5p), which functions as a tumor suppressor, has been reported to be downregulated in colorectal cancer (CRC) tissues and to be associated with cancer invasion. However, the detailed regulatory mechanism of curcumol in the malignant progression of CRC remains unknown. MTT, Transwell, scratch, western blotting and reverse transcription-quantitative PCR assays were performed to examine how curcumol inhibited CRC cell viability, invasion and migration, and to detect the role of miR-30a-5p and curcumol in the invasion and Hippo signaling pathways of CRC cells. The present study revealed that miR-30a-5p expression was downregulated in human CRC tissues and cells. The results demonstrated that miR-30a-5p downregulation was accompanied by the inactivation of the Hippo signaling pathway, which was demonstrated to promote CRC cell viability, invasion and migration. Curcumol treatment was identified to increase miR-30a-5p expression and to activate the Hippo signaling pathway, which in turn inhibited the invasion and migration of CRC cells. Overexpression of miR-30a-5p enhanced the effects of curcumol on cell invasion and migration, and the Hippo signaling pathway in CRC cells. Furthermore, downregulation of miR-30a-5p reversed the effects of curcumol on cell invasion and migration, and the Hippo signaling pathway in CRC cells. These findings identified novel signaling pathways associated with miR-30a-5p and revealed the effects of curcumol on miR-30a-5p expression. Therefore, curcumol may serve as a potential therapeutic strategy to delay CRC progression. [ABSTRACT FROM AUTHOR]

Renal ischemia/reperfusion (I/R) injury often occurs during multiple organ failure and sepsis, and autophagy may serve a role in I/R injury. The aim of the present study was to explore the effect of microRNA (miR)‑30a‑5p on autophagy in renal I/R injury. miR‑30a‑5p and autophagy‑related protein expression levels in renal I/R injury mouse models and in hypoxia/re‑oxygenation HK‑2 cell models were determined using reverse transcription‑quantitative PCR or western blotting; apoptosis was analyzed using flow cytometry. The effects of miR‑30a‑5p, Beclin‑1 and autophagy‑related gene 16 (ATG16) on the proliferation and autophagy of HK‑2 cells were analyzed through gain‑ and loss‑of‑function studies. miR‑30a‑5p expression was significantly decreased after renal I/R injury in the in vivo and in vitro experiments. Renal I/R injury led to upregulated expression of autophagy‑related proteins microtubule‑associated protein light chain 3 (LC3)‑Ⅱ and Beclin‑1, and downregulated expression of p62. miR‑30a‑5p overexpression decreased the number of LC3 punctae, decreased HK‑2 cell apoptosis, increased p62 expression and decreased LC3‑Ⅱ and Beclin‑1 expression. Inhibition of miR‑30a‑5p exhibited the opposite effects. A luciferase reporter assay demonstrated that miR‑30a‑5p targeted Beclin‑1. Beclin‑1 overexpression led to a significant increase in LC3‑Ⅱ expression and a decrease in p62 expression, as well as a significant increase in apoptosis. Beclin‑1 overexpression also increased the protein expression level of ATG16. Downregulation of Beclin‑1 decreased the expression of LC3‑Ⅱ, elevated the p62 level and decreased apoptosis. ATG16 knockdown showed similar effects as those of Beclin‑1 downregulation. In conclusion, miR‑30a‑5p was increased in renal I/R injury and might mitigate autophagy by regulating the Beclin‑1/ATG16 pathway.

Viral myocarditis (VMC) is a life-threatening disease characterized by severe cardiac inflammation generally caused by coxsackievirus B3 (CVB3) infection. Several microRNAs (miRNAs or miRs) are known to play crucial roles in the pathogenesis of VMC. The study aimed to decipher the role of miR-30a-5p in the underlying mechanisms of VMC pathogenesis. We first quantified miR-30a-5p expression in a CVB3-induced mouse VMC model. The physiological characteristics of mouse cardiac tissues were then detected by hematoxylin and eosin (HE) and Picrosirius red staining. We established the correlation between miR-30a-5p and SOCS1, using dual-luciferase gene assay and Pearson's correlation coefficient. The expression of inflammatory factors (IFN-γ, IL-6, IL-10, and IL-13), M1 polarization markers [TNF-α, inducible nitric oxide synthase (iNOS)], M2 polarization markers (Arg-1, IL-10), and myocardial hypertrophy markers [atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)] was detected by RT-qPCR and Western blot analysis. miR-30a-5p was found to be highly expressed in VMC mice. Silencing of miR-30a-5p improved the cardiac function index and reduced heart weight-to-body weight ratio, myocardial tissue pathological changes and fibrosis degree, serological indexes, as well as proinflammatory factor levels, while enhancing anti-inflammatory factor levels in VMC mice. Furthermore, silencing of miR-30a-5p inhibited M1 polarization of macrophages while promoting M2 polarization in vivo and in vitro. SOCS1 was a target gene of miR-30a-5p, and the aforementioned cardioprotective effects of miR-30a-5p silencing were reversed upon silencing of SOCS1. Overall, this study shows that silencing of miR-30a-5p may promote M2 polarization of macrophages and improve cardiac injury following VMC via SOCS1 upregulation, constituting a potential therapeutic target for VMC treatment. NEW & NOTEWORTHY We found in this study that microRNA (miR)-30a-5p inhibition might improve cardiac injury following viral myocarditis (VMC) by accelerating M2 polarization of macrophages via SOCS1 upregulation. Furthermore, the anti-inflammatory mechanisms of miR-30a-5p inhibition may contribute to the development of new therapeutic strategies for VMC.

Exosomes carrying microRNAs (miRNAs) have been demonstrated to play critical roles in the regulation of development, growth and metastasis of cancer. Bioinformatic predictions identified differentially expressed SRY-box 9 (SOX9) in OC, and the regulatory miRNA miR-139-5p. Here, we aim to evaluate the function of exosomal miR-139-5p in the sensitivity of ovarian cancer (OC) cells to cis-diamminedichloroplatinum(II) (DDP). Expression pattern of miR-139-5p and SOX9 in ovarian cancer cells (SKOV3) and DDP-resistant cells (SKOV3/DDP) was identified using reverse transcription quantitative polymerase chain reaction and western blot analysis. The relationship between miR-139-5p and SOX9 was validated using a dual-luciferase reporter assay. SKOV3/DDP cell line was developed and introduced with miR-30a-5p mimic to analyse the effects of miR-30a-5p on resistance to DDP. The in vitro and in vivo effects of exosomal miR-30a-5p on resistance of SKOV3 cells to DDP were assessed in a co-culture system of exosomes and OC cells as well as in tumour-bearing nude mice. High expression of SOX9 and low expression of miR-30-5p were witnessed in OC. Furthermore, miR-30-5p, a downregulated miRNA in SKOV3/DDP cells, increased the rate of cell apoptosis and enhanced the sensitivity of SKOV3/DDP cells to DDP by targeting SOX9. Moreover, exosomes carrying miR-30a-5p were identified to sensitize SKOV3/DDP cells to DDP both in vitro and in vivo . These data together supported an important conclusion that DDP-resistant OC cell-derived exosomal miR-30a-5p enhanced cellular sensitivity to DDP, highlighting a potential strategy to overcome drug resistance.

MicroRNAs (miRs) are a class of small non-coding RNAs of 18-25 nucleotides in length that serve as key regulators in the development and progression of human cancers. Recently, miR-30b-5p, as a member of the miR-30 family, has been reported to act as a tumor suppressor in gastric cancer. However, the expression and function of miR-30a-5p in gastric cancer, as well as the corresponding underlying mechanism, remain unknown. In the present study, it was demonstrated that the expression of miR-30a-5p was significantly reduced in gastric cancer tissues (n=43) compared with normal gastric tissues (n=10; P<0.01). Similarly, miR-30a-5p was significantly downregulated in the gastric cancer cell lines AGS, HGC27, BGC823 and SGC7901, when compared with the normal gastric mucosa epithelial cell line GES-1 (P<0.01). In addition, overexpression of miR-30a-5p significantly inhibited the proliferation and invasion of AGS cells (P<0.01). Insulin-like growth factor 1 receptor (IGF-1R) was identified as a novel target of miR-30a-5p, and the protein expression of IGF-1R was negatively regulated by miR-30a-5p in AGS cells (P<0.01). Furthermore, overexpression of IGF-1R significantly reversed the inhibitory effect of miR-30a-5p on the proliferation and invasion of AGS cells (P<0.01), indicating that IGF-1R was involved in miR-30a-5p-mediated proliferation and invasion of AGS cells. It was also observed that the expression of IGF-1R mRNA was upregulated in gastric cancer tissues compared with normal gastric tissues (P<0.01), and its levels of expression were reversely correlated with that of miR-30a-5p in gastric cancer tissues (R 2 =0.3892; P<0.01). Collectively, these data suggest that miR-30a-5p inhibits the growth and metastasis of gastric cancer by directly targeting IGF-1R. Therefore, the miR-30a-5p/IGF-1R axis may be a potential therapeutic target in the treatment of gastric cancer.

The present study aimed to explore the expression of microRNA (miRNA or miR) in drug-resistant and drug-sensitive ovarian cancer cell lines, and to seek the potential therapeutic target of ovarian cancer drug-resistant mechanism in order to improve drug resistance by altering miRNA levels. The drug-resistant characteristics of SKOV3/DDP, SKOV3, COC1/DDP and COC1 cell lines were studied. The miRNAs that were differentially expressed between cisplatin-resistant cells and its parental cells in ovarian cancer were screened with a miRNA chip. The effect of miRNAs was detected, and their drug-resistant mechanism was investigated by transfection and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide methods. Among the expression screening of miRNAs, 41 mRNAs, including Homo sapiens (hsa)-miR-30a-5p and hsa-miR-34c-5p, were highly expressed in the drug-resistant cells, whereas 44 miRNAs, including hsa-miR-96-5p and hsa-miR-200c-3p, were lowly expressed. The expression levels of hsa-miR-30a-5p in two types of ovarian cancer chemotherapy-resistant cell lines were significantly higher than those in chemotherapy-sensitive cell lines, which was associated with ovarian cancer chemotherapy resistance. In conclusion, high expression of miRNA-30a-5p was able to promote cell growth and colony forming ability, and enhance cell migration and invasion. Thus, miRNA-30a-5p is expected to become a meaningful novel target for ovarian cancer resistant treatment.