MiR‑500a‑5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5

Li, Yong; Su, Dan; Qi, Xiaojuan; Ma, Jing

doi:10.3892/mmr.2018.9259

Cited by 8 publications

(10 citation statements)

References 31 publications

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“…The results indicated that the lncRNA NEAT1 might suppress the development of gastric cancer by promoting gastric cancer cell apoptosis. Previous studies have identified miR-500a-3p as a potential prognostic predictor in certain types of cancer, including hepatocellular carcinoma and glioblastoma, and have reported an association between miR-500a and TNM stage in lung cancer and conjunctival malignant melanoma (32)(33)(34)(35). Other studies have reported that XBP-1 is closely associated with clinical outcome (36,37).…”

Section: Discussionmentioning

confidence: 99%

lncRNA NEAT1 regulates gastric carcinoma cell proliferation, invasion and apoptosis via the miR‑500a‑3p/XBP‑1 axis

et al. 2021

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Gastric cancer is a serious malignant tumor. Despite progression in gastric cancer research in recent years, the specific molecular mechanism underlying the pathogenesis of the disease is not completely understood. Long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) affects the proliferation and metastasis of multiple types of tumor cells in colorectal cancer and breast cancer but its specific role in gastric cancer requires further investigation. The aim of the present study was to analyze the role of NEAT1 in gastric cancer. The expression of endoplasmic reticulum stress marker proteins and apoptosis-related proteins in gastric cancer tissue and cell lines was analyzed using western blotting. The targeting relationship of NEAT1 and miR-500a-3p was analyzed using dual-luciferase reporter assay. Cell proliferation was analyzed using CCK8 assay and colony formation assay while cell invasion was detected using Transwell assay. Cell apoptosis was analyzed using TUNEL staining and LC3 expression through immunofluorescent staining (IF). The results showed that lncRNA NEAT1-overexpression gastric cancer cells were established to determine its effects on cell proliferation, invasion, apoptosis, autophagy and endoplasmic reticulum stress. Subsequently, microRNA (miR)-500a was overexpressed in lncRNA NEAT1-overexpression cells. Compared with the vector group, lncRNA NEAT1 overexpression significantly inhibited gastric cancer cell proliferation and invasion, but significantly promoted cell apoptosis. Furthermore, the results indicated that lncRNA NEAT1 targeted and downregulated the expression of miR-500a-3p, and miR-500a-3p targeted X-box binding protein-1 (XBP-1) mRNA. lncRNA NEAT1 overexpression-mediated inhibition of gastric cancer cell proliferation and invasion was significantly reversed by miR-500a-3p overexpression. Furthermore, compared with the vector group, the expression levels of endoplasmic reticulum stress-related proteins (XBP-1S/XBP-1U ratio and 78-kDa glucose-regulated protein) and apoptosis-related proteins (Bax and cleaved-caspase-3) were significantly upregulated by lncRNA NEAT1 overexpression; however, miR-500a-3p overexpression reversed lncRNA NEAT1 overexpression-mediated effects on protein expression. The present study demonstrated that lncRNA NEAT1 inhibited gastric cancer cell proliferation and invasion, and promoted apoptosis by regulating the miR-500a-3p/XBP-1 axis.

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Section: Discussionmentioning

confidence: 99%

lncRNA NEAT1 regulates gastric carcinoma cell proliferation, invasion and apoptosis via the miR‑500a‑3p/XBP‑1 axis

et al. 2021

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“…Our data showed that miR‐500a‐5p was decreased in MN tissues. CXCL16 has been reported to be increased in patients with chronic kidney diseases 13 . Subsequently, the expression of CXCL16 was also examined in MN tissues.…”

Section: Discussionmentioning

confidence: 99%

“…It has been revealed that miR‐500a‐5p inhibits cell growth in human colorectal cancer 12 . In glioblastoma, miR‐500a‐5p enhances cell proliferation and metastasis, 13 whereas the role of miR‐500a‐5p in podocyte apoptosis and whether miR‐500a‐5p participates in circ_0000524‐mediated function need be further addressed. The upregulation of C‐X‐C chemokine ligand 16 (CXCL16) is related to the development of chronic kidney disease 14 .…”

Section: Introductionmentioning

confidence: 99%

Circ_0000524/miR‐500a‐5p/CXCL16 axis promotes podocyte apoptosis in membranous nephropathy

Sun

et al. 2020

Eur J Clin Investigation

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Background Podocytes apoptosis is a hallmark of membranous nephropathy (MN). Circ_0000524 has been reported to be associated with patients with MN, whereas the effect of circ_0000524 on podocytes apoptosis and the underlying mechanisms in MN have not been elaborated. Methods Quantitative real‐time polymerase chain reaction (qRT‐PCR) and Western blot were performed to detect the expressions of circ_0000524, microRNA‐500a‐5p (miR‐500a‐5p), and C‐X‐C chemokine ligand 16 (CXCL16) in MN tissues and podocytes. Podocyte injury was induced by angiotensin II (AngII). Cell apoptosis was detected by flow cytometry. Caspase‐3 or caspase‐9 activity was evaluated using a caspase‐3 or caspase‐9 activity assay kit, respectively. Dual‐luciferase reporter assay, RNA immunoprecipitation (RIP) and pull‐down assay were used to address the relationship among circ_0000524,miR‐500a‐5p and CXCL16. Results Upregulation of circ_0000524 and CXCL16 and low expression of miR‐500a‐5p were observed in MN tissues. AngII treatment induced the overexpression of circ_0000524 and CXCL16, a decrease of miR‐500a‐5p, and induced cell apoptosis in podocytes. Circ_0000524 negatively modulated the expression of miR‐500a‐5p. Circ_0000524 depletion inhibited podocyte apoptosis, which was rescued by loss of miR‐500a‐5p. miR‐500a‐5p contained the binding sites with CXCL16. Circ_0000524 knockdown hampered CXCL16 expression by upregulating miR‐500a‐5p expression. Additionally, miR‐500a‐5p upregulation suppressed AngII‐induced podocyte apoptosis, which was rescued by enhanced expression of CXCL16. Conclusion Circ_0000524/miR‐500a‐5p/CXCL16 pathway regulated podocyte apoptosis in MN.

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Section: Discussionmentioning

confidence: 99%

“… 21 Xia et al 22 have confirmed that miR-1908 could facilitate cell proliferation and migration by suppressing PTEN tumor suppressor pathway in GBM. Liu et al 23 have reported that miR-500a-5p could accelerate the proliferation, migration and invasion through targeting chromodomain helicase DNA binding protein 5 in GBM. In this study, we demonstrated that miR-6071 could significantly suppress proliferation, migration and invasion, and also facilitate apoptosis in U251 and A172 cells.…”

Section: Discussionmentioning

confidence: 99%

<p>MicroRNA-6071 Suppresses Glioblastoma Progression Through the Inhibition of PI3K/AKT/mTOR Pathway by Binding to ULBP2</p>

Zhou

An²,

2020

OTT

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The purpose of this study was to explore the effect of microRNA-6071 (miR-6071) on glioblastoma (GBM) and its potential mechanisms. Methods: In this study, the expressions of miR-6071 and UL16 binding protein 2 (ULBP2) were measured by qRT-RCR in GBM tissues and cells. The prognostic values of miR-6071 and ULBP2 were evaluated by Kaplan-Meier methods using the data obtained from The Cancer Genome Atlas (TCGA) database. The cell clones, proliferation, apoptosis, migration and invasion in GBM cells were detected by colony formation assay, EdU assay, flow cytometry, wound-healing assay and transwell assay. The targeting relationship between miR-6071 and ULBP2 was predicted by Targetscan 7.2 and further verified by dualluciferase reporter gene assay. Moreover, the expressions of Bax, caspase-3, Bcl-2, matrix metalloproteinases 2 (MMP-2), MMP-9, phosphatidylinositol 3′-kinase (PI3K), p-PI3K, protein kinase B (AKT), p-AKT, mammalian target of rapamycin (mTOR) and p-mTOR were measured by Western blot. Results: miR-6071 was lowly expressed and ULBP2 was highly expressed in GBM tissues and cells. miR-6071 significantly repressed the proliferation, migration and invasion, and promoted apoptosis in GBM cells. Moreover, miR-6071 also inhibited the activation of PI3K/AKT/mTOR pathway in GBM cells. Additionally, miR-6071 has been shown to negatively regulate ULBP2 expression. We also confirmed that ULBP2 could reverse the effects of miR-6071 on GBM cells through regulating PI3K/AKT/mTOR pathway. Conclusion: Our study demonstrated that miR-6071 could suppress cell proliferation, migration and invasion, as well as promote apoptosis through the inhibition of PI3K/Akt/ mTOR pathway by binding to ULBP2 in GBM.

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MiR‑500a‑5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5

Cited by 8 publications

References 31 publications

lncRNA NEAT1 regulates gastric carcinoma cell proliferation, invasion and apoptosis via the miR‑500a‑3p/XBP‑1 axis

lncRNA NEAT1 regulates gastric carcinoma cell proliferation, invasion and apoptosis via the miR‑500a‑3p/XBP‑1 axis

Circ_0000524/miR‐500a‐5p/CXCL16 axis promotes podocyte apoptosis in membranous nephropathy

<p>MicroRNA-6071 Suppresses Glioblastoma Progression Through the Inhibition of PI3K/AKT/mTOR Pathway by Binding to ULBP2</p>

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