LncRNA SNHG14 contributes to the progression of NSCLC through miR‐206/G6PD pathway

Zhao, Lin; Zhang, Xiaodong; Shi, Yantong; Teng, Tianlu

doi:10.1111/1759-7714.13374

Cited by 16 publications

(16 citation statements)

References 22 publications

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“…Zhao et al indicated miR-206 inhibited cell viability, colony-forming ability and metastasis in NSCLC. 29 MiR-206 also participated in regulation in cancer progression under hypoxia. Tan et al unveiled miR-206 expression was downregulated in thyroid carcinoma tissues, cells and hypoxia-mediated thyroid carcinoma, and its inhibitor restrained the inhibition effects of nuclear paraspeckle assembly transcript 1 on hypoxia-mediated cell migration and invasion anaplastic thyroid carcinoma cells, 30 which meant that miR-206 suppressed cell migration and invasion under hypoxia.…”

Section: Discussionmentioning

confidence: 99%

CircASXL1 Knockdown Restrains Hypoxia-Induced DDP Resistance and NSCLC Progression by Sponging miR-206

Yu¹,

Li²,

Peng³

et al. 2021

CMAR

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Background Non-small cell lung carcinoma (NSCLC) is a primary prevalent type of cancer in people worldwide. Cisplatin (DDP) has been widely used to treat NSCLC; however, its curative effect was restrained under hypoxia. In this study, the effects of hypoxia treatment on DDP resistance and NSCLC progression and underneath mechanism were revealed. Methods The expression of circular RNA ASXL1 (circASXL1) and microRNA-206 (miR-206) in NSCLC tissues, cells and hypoxia-mediated NSCLC cells was determined by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of proliferation, metastasis and apoptosis-related proteins, drug resistance-related protein and hypoxia-inducible factor-1alpha (HIF-1α) protein was detected by Western blot. The effects of circASXL1 knockdown on hypoxia-induced DDP resistance and NSCLC progression were revealed by cell counting kit-8 proliferation (CCK-8), cell colony formation, transwell and flow apoptosis assays. RNA immunoprecipitation (RIP) assay was performed to determine whether circASXL1 could form silence-inducing complexes with miRNA. The associated relationship between circASXL1 and miR-206 was predicted by circBank online database, and identified by RNA pull-down and dual-luciferase reporter assays. The effects between circASXL1 knockdown and miR-206 downregulation on tumor growth in vivo were investigated by in vivo tumor formation assay. Results CircASXL1 expression was dramatically upregulated, whereas miR-206 was significantly down-regulated in NSCLC tissues, cells and hypoxia-mediated NSCLC cells as compared to control groups. CircASXL1 knockdown reversed hypoxia-mediated promotion effects on DDP resistance, cell proliferation, migration, and invasion, and inhibition impact on cell apoptosis, whereas these effects were restored by miR-206 inhibitor. Additionally, circASXL1 was found to form silence-inducing complexes with miRNA and act as a sponge of miR-206. CircASXL1 silencing downregulated HIF-1α expression by controlling miR-206 expression. Furthermore, circASXL1 silencing repressed tumor growth in vivo by sponging miR-206. Conclusion CircASXL1 knockdown inhibited DDP resistance, cell proliferation, migration and invasion, whereas induced cell apoptosis under hypoxia by associating with miR-206 in NSCLC. This study provides a new sight in treating NSCLC with DDP under hypoxia.

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Section: Discussionmentioning

confidence: 99%

CircASXL1 Knockdown Restrains Hypoxia-Induced DDP Resistance and NSCLC Progression by Sponging miR-206

Yu¹,

Li²,

Peng³

et al. 2021

CMAR

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“…Surveys such as that conducted by Zhao et al have shown that SNHG14 is highly expressed in non-small cell lung cancer cells. SNHG14 participates in the cell proliferation, invasion and migration of non-small cell lung cancer cells by regulating miR-206/G6PD [17]. As an oncogene in prostate cancer, SNHG14 contributes to the progression of prostate cancer by sponging miR-613 [18].…”

Section: Discussionmentioning

confidence: 99%

LncRNA SNHG14 promotes OGD/R-induced neuron injury by inducing excessive mitophagy via miR-182-5p/BINP3 axis in HT22 mouse hippocampal neuronal cells

Deng

Ren

et al. 2020

Biol Res

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Background Long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) is associated with cerebral ischemia–reperfusion (CI/R) injury. This work aims to explore the role of SNHG14 in CI/R injury. Methods HT22 (mouse hippocampal neuronal cells) cell model was established by oxygen–glucose deprivation/reoxygenation (OGD/R) treatment. The interaction among SNHG14, miR-182-5p and BNIP3 was verified by luciferase reporter assay. Flow cytometry, western blot and quantitative real-time PCR were performed to examine apoptosis, the expression of genes and proteins. Results SNHG14 and BNIP3 were highly expressed, and miR-182-5p was down-regulated in the OGD/R-induced HT22 cells. OGD/R-induced HT22 cells exhibited an increase in apoptosis. SNHG14 overexpression promoted apoptosis and the expression of cleaved-caspase-3 and cleaved-caspase-9 in the OGD/R-induced HT22 cells. Moreover, SNHG14 up-regulation enhanced the expression of BNIP3, Beclin-1, and LC3II/LC3I in the OGD/R-induced HT22 cells. Furthermore, SNHG14 regulated BNIP3 expression by sponging miR-182-5p. MiR-182-5p overexpression or BNIP3 knockdown repressed apoptosis in OGD/R-induced HT22 cells, which was abolished by SNHG14 up-regulation. Conclusion Our study demonstrates that lncRNA SNHG14 promotes OGD/R-induced neuron injury by inducing excessive mitophagy via miR-182-5p/BINP3 axis in HT22 mouse hippocampal neuronal cells. Thus, SNHG14/miR-182-5p/BINP3 axis may be a valuable target for CI/R injury therapies.

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“…The mechanism of miR-206 downregulated by BANCR was unclear. Several studies have reported that long non-coding RNA MIR4435-2HG, SNHG14 and LINC00707 can directly bind miR-206 to suppress it expression [26][27][28]. Therefore, we speculated BANCR decreased the miR-206 expression was involved in regulating these LncRNA expression.…”

Section: Discussionmentioning

confidence: 87%

LncRNA BANCR Facilitates Melanoma Cells Growth, Migration and Invasion by Inhibiting miR-206 and miR-571 to Induce G6PD Expression

Yang¹,

Yang²,

Zhang³

et al. 2020

Preprint

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Background Here, we evaluated the roles of LncRNA BANCR in facilitating melanoma cells growth, migration, invasion. Moreover, we examined the molecular mechanisms of BANCR in promoting melanoma development.Methods Here, we measured BANCR expression by quantitative PCR. By transwell assay, we detected the cancer cell migration and invasion. The melanoma growth and migration induced by BANCR was detected by colony formation assay and in xenograft nude mice model. By Western blotting and luciferase assay, we evaluated the molecular mechanism of BANCR in inhibiting miR-206 and miR-571 to induce G6PD expression. Results We found BANCR was overexpressed in melanoma cells and tissues. In addition, we showed that BANCR promoted melanoma cells growth in vitro and in vivo. Moreover, BANCR promotes cancer cell migration and invasion in vitro, and induced melanoma metastasis in nude mice model. The migration and invasion induced by BANCR in melanoma cells were involved in upregulation of matrix metalloproteinases (MMPs) MMP2 and MMP9. Mechanismly, we indicated BANCR promoted melanoma cell growth and migration by suppressing miR-206 and miR-571 expression to activate glucose metabolism pathway and induce G6PD expression. Furthermore, miR-206 and miR-571 inhibited G6PD expression by directly binding the 3’UTR of G6PD. We also showed miR-206 and miR-571 inhibited the proliferation of melanoma cells.Conclusion Our findings indicated that BANCR contributed to melanoma development, which might provide novel insights into the function of lncRNA-driven carcinogenesis in melanoma.

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LncRNA SNHG14 contributes to the progression of NSCLC through miR‐206/G6PD pathway

Cited by 16 publications

References 22 publications

CircASXL1 Knockdown Restrains Hypoxia-Induced DDP Resistance and NSCLC Progression by Sponging miR-206

CircASXL1 Knockdown Restrains Hypoxia-Induced DDP Resistance and NSCLC Progression by Sponging miR-206

LncRNA SNHG14 promotes OGD/R-induced neuron injury by inducing excessive mitophagy via miR-182-5p/BINP3 axis in HT22 mouse hippocampal neuronal cells

LncRNA BANCR Facilitates Melanoma Cells Growth, Migration and Invasion by Inhibiting miR-206 and miR-571 to Induce G6PD Expression

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