miR-30c Impedes Glioblastoma Cell Proliferation and Migration by Targeting SOX9

Liu, Shihui; Li, Xiuxiu; Zhuang, Sujing

doi:10.3727/096504018x15193506006164

Cited by 32 publications

(18 citation statements)

References 29 publications

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“…34 Due to the characteristic of multiple targets of miRNAs, miR-30c has also been reported to target other genes, such as SOX9, BCL9, and CTGF. 25,35,36 In this work, to determine the interaction between MALAT1 and miR-30c, miR-30c, and NLRP3, we In conclusion, this study highlighted the mutual regulation between MALAT1 and miR-30c, miR-30c, and NLRP3 in regulating renal tubular epithelial cell pyroptosis of DN. This research could contribute to a better understanding of the pathogenesis of DN and help to find out the effective treatment for DN.…”

Section: Discussionmentioning

confidence: 66%

LncRNA MALAT1 promoted high glucose‐induced pyroptosis of renal tubular epithelial cell by sponging miR‐30c targeting for NLRP3

Liu

Zhuo

et al. 2020

The Kaohsiung J of Med Scie

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Diabetic nephropathy (DN), characterized by the chronic loss of kidney function during diabetes, is a long‐term kidney disease that affects millions of populations. However, the etiology of DN remains unclear. DN cell model was established by treating HK‐2 cells with high glucose (HG) in vitro. Expression of metastasis‐associated lung adenocarcinoma transcript‐1 (MALAT1), miR‐30c, nucleotide binding and oligomerization domain‐like receptor protein 3 (NLRP3), caspase‐1, IL‐1β, and IL‐18 in treated HK‐2 cells were tested by quantitative polymerase chain reaction. HK‐2 cell pyroptosis was assessed using flow cytometry analysis. Lactate dehydrogenase (LDH) activity was examined with a LDH assay kit. Correlation among MALAT1, miR‐30c, and NLRP3 was examined via dual‐luciferase reporter assay. Here, we revealed that MALAT1 was upregulated, but miR‐30c was downregulated in HG‐treated HK‐2 cells, leading to upregulation of NLRP3 expression and cell pyroptosis. Knockdown of MALAT1 or overexpression of miR‐30c protected HK‐2 cells from HG‐induced pyroptosis. Meanwhile, we found that MALAT1 promoted NLRP3 expression by sponging miR‐30c through dual‐luciferase reporter assay. Moreover, the co‐transfection of sh‐MALAT1 and miR‐30c inhibitor could reverse the protective effects of the sh‐MALAT1 on the HG‐induced pyroptosis. These results confirmed that MALAT1 regulated HK‐2 cell pyroptosis by inhibiting miR‐30c targeting for NLRP3, contributing to a better understanding of DN pathogenesis and help to find out the effective treatment for DN.

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Section: Discussionmentioning

confidence: 66%

LncRNA MALAT1 promoted high glucose‐induced pyroptosis of renal tubular epithelial cell by sponging miR‐30c targeting for NLRP3

Liu

Zhuo

et al. 2020

The Kaohsiung J of Med Scie

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“…In Song's research, miR-30c could be use as the potential biomarkers for the diagnosis and prognosis of prostate cancer patients and the detection of miRNAs including miR-30c is an effective way to predict patient's prognosis and evaluate the therapeutic efficacies [63].Liu found that miR-30c impedes glioblastoma cell proliferation and migration by targeting SOX9.In their study, they found that the expression levels of miR-30c were significantly downregulated in glioblastoma tissues and cancer cell lines. This research also found that after miR-30c overexpression, the majority of glioblastoma cells were arrested in G0 phase and miR-30c over-expression suppressed the migration and invasion abilities of glioblastoma cells [64]. Ma reported miR-30c functions as a tumor suppressor via targeting SNAI1 in esophageal squamous cell carcinoma (ESCC).…”

Section: The Cellular Molecular and Drug-resistance Mechanisms Of MImentioning

confidence: 74%

Role of MicroRNA-30c in cancer progression

et al. 2020

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MicroRNAs (miRNAs or miRs) is a non-coding small RNA of a type of 18~24 nucleotide-regulated gene that has been discovered in recent years. It mainly degrades the target gene mRNA or inhibits its translation process through the complete or incomplete bindings with 3'UTR of target genes, followed by the regulation of individual development, apoptosis, proliferation, differentiation and other life activities through the post-transcriptional regulation. Among many miRNAs, the microRNA family, miR-30, plays diverse roles in these key process of neoplastic transformation, metastasis, and clinical outcomes in different cancer progression. As key member of miR-30, miR-30c is regulated by oncogenic transcription factors and cancer progression related genes. Recently, numerous studies have demonstrated that the aberrant expression of miR-30c was significantly associated with the majority of human cancer progression. In this review, the diverse roles of miR-30c in different cancer progression such as the cellular and molecular mechanisms, the potential applications in clinics were summarized to speculate the benefits of miR-30c over-expression in cancer treatment and prognosis.

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“…Previous studies reported that SOX9 could be directly targeted by multiple miRNAs. For instance, miR-14541 and miR-30c42 directly interacted with SOX9 and decreased its expression in GBM cells, thus resulting in the suppression of GBM progression. Accordingly, SOX9 knockdown using miRNAs-based gene therapy might represent a potential therapeutic approach for the management of GBM patients.…”

Section: Discussionmentioning

confidence: 99%

<p>microRNA-605 directly targets SOX9 to alleviate the aggressive phenotypes of glioblastoma multiforme cell lines by deactivating the PI3K/Akt pathway</p>

Jia

Wang

Yin

et al. 2019

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Background Aberrant microRNA (miRNA) expression has been widely reported to play a crucial role in the progression and development of glioblastoma (GBM). miR-605 has been identified as a tumor-suppressing miRNA in several types of human cancers. Nevertheless, the expression profile and detailed roles of miR-605 in GBM remain unclear and need to be further elucidated. Materials and methods RT-qPCR analysis was utilized for the determination of miR-605 expression in GBM tissues and cell lines. In addition, CCK-8 assay, transwell migration and invasion assays, as well as sub-cutaneous xenograft mouse models were utilized to evaluate the effects of miR-605 upregulation in GBM cells. Notably, the potential mechanisms underlying the activity of miR-605 in the malignant phenotypes of GBM were explored. Results We observed that expression of miR-605 was reduced in GBM tissues and cell lines. Decreased miR-605 expression exhibited significant correlation with KPS score. The overall survival rate in GBM patients with low miR-605 expression was lower than that of patients with high miR-605 expression. Increased miR-605 expression suppressed the proliferation, migration, and invasion of U251 and T98 cells. In addition, miR-605 upregulation impaired tumor growth in vivo. Furthermore, SRY-Box 9 (SOX9) was identified as a direct target gene of miR-605 in U251 and T98 cells. SOX9 expression was shown to exhibit an inverse correlation with miR-605 expression in GBM tissues. Moreover, silencing of SOX9 expression mimicked the tumor-suppressing roles of miR-605 in U251 and T98 cells, while SOX9 restoration rescued the suppressive effects of miR-605 overexpression in the same. Notably, miR-605 suppressed the PI3K/Akt pathway in GBM in vitro and in vivo. Conclusion These results demonstrated that miR-605 acts as a tumor suppressor in the development of GBM by directly targeting SOX9 and inhibiting the activation of the PI3K/Akt pathway, suggesting its potential role as a therapeutic target for GBM.

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miR-30c Impedes Glioblastoma Cell Proliferation and Migration by Targeting SOX9

Cited by 32 publications

References 29 publications

LncRNA MALAT1 promoted high glucose‐induced pyroptosis of renal tubular epithelial cell by sponging miR‐30c targeting for NLRP3

LncRNA MALAT1 promoted high glucose‐induced pyroptosis of renal tubular epithelial cell by sponging miR‐30c targeting for NLRP3

Role of MicroRNA-30c in cancer progression

<p>microRNA-605 directly targets SOX9 to alleviate the aggressive phenotypes of glioblastoma multiforme cell lines by deactivating the PI3K/Akt pathway</p>

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