Circ_0006332 promotes growth and progression of bladder cancer by modulating MYBL2 expression via miR-143

Li, Mingshan; Liu, Yili; Liu, Jie; Li, Wei; Li, Ning; Xue, Dongwei; Zhang, Xiling; Wang, Ping

doi:10.18632/aging.102481

Cited by 19 publications

(14 citation statements)

References 36 publications

(32 reference statements)

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“…Furthermore, MYBL2 was one direct gene of miR‐423‐5p and elevated expression of miR‐423‐5p suppressed MYBL2 expression and ectopic expression of RPSAP52 increased MYBL2 expression in SCC‐4 cell. A previous study indicated that MYBL2 acted as one oncogene in tumour development 44,45 . Finally, we illustrated that RPSAP52 overexpression promoted TSCC cell growth and cycle and induced cytokine secretion including IFN‐γ, IL‐1β and IL‐6, IL‐8, IL‐10 and TGF‐β via modulating MYBL2.…”

Section: Discussionsupporting

confidence: 55%

lncRNA RPSAP52 induced the development of tongue squamous cell carcinomas via miR‐423‐5p/MYBL2

Gong

et al. 2021

J Cellular Molecular Medi

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Growing lncRNAs have been noted to involve in the initiation and development of several tumours including tongue squamous cell carcinomas (TSCCs). However, the biological role and mechanism of lncRNA RPSAP52 were not well‐explained. We indicated that RPSAP52 was higher in TSCC samples compared with that in control samples. The higher expression of RPSAP52 was positively correlated with higher T stage and TNM stage. Ectopic expression of RPSAP52 induced TSCC cell growth and cycle and induced cytokine secretion including IFN‐γ, IL‐1β and IL‐6, IL‐8, IL‐10 and TGF‐β. We found that the overexpression of RPSAP52 suppressed miR‐423‐5p expression in SCC‐4 cell. miR‐423‐5p was lower in TSCC samples compared with that in control samples, and miR‐423‐5p level was negatively correlated with higher T stage and TNM stage. Pearson's correlation indicated that miR‐423‐5p was negatively associated with that of RPSAP52 in TSCC tissues. Furthermore, MYBL2 was one direct gene of miR‐423‐5p and elevated expression of miR‐423‐5p suppressed MYBL2 expression and ectopic expression of RPSAP52 increased MYBL2 expression in SCC‐4 cell. Finally, we illustrated that RPSAP52 overexpression promoted TSCC cell growth and cycle and induced cytokine secretion including IFN‐γ, IL‐1β and IL‐6, IL‐8, IL‐10 and TGF‐β via modulating MYBL2. These data provided new insight into RPSAP52, which may be one potential treatment target for TSCC.

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Section: Discussionsupporting

confidence: 55%

lncRNA RPSAP52 induced the development of tongue squamous cell carcinomas via miR‐423‐5p/MYBL2

Gong

et al. 2021

J Cellular Molecular Medi

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“… 11 , 12 For instance, Li et al indicated that circ_006332 contributed to bladder cancer development by regulating MYB Proto-Oncogene Like 2 expression. 13 Zhang et al also revealed that circ-phosphoglycerate mutase 1(circ-PGAM) promoted ovarian cancer growth via sponging microRNA-542-3p (miR-542-3p). 14 In addition, Xu et al demonstrated that circ_0004771 could regulate hypoxia-mediated 5-Fluorouracil resistance to gastric cancer.…”

Section: Introductionmentioning

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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“…Circular RNA (circRNA) is a noncoding RNA with closed loop. 7 An increasing number of studies have indicated that circRNA acted as a promoter or suppressor in cancer progression. 8,9 For instance, Yang et al revealed that circ_0049027 (circ_HuR) inhibited cell migration and invasion in vitro and in vivo; 8 Wu et al also explained that circ-ZNF609 contributed to the proliferation of colorectal cancer cells by sponging microRNA-150 (miR-150).…”

Section: Introductionmentioning

confidence: 99%

<p>Gambogic Acid Inhibits the Progression of Gastric Cancer via circRNA_ASAP2/miR-33a-5p/CDK7 Axis</p>

Lin¹,

Lin²,

He³

et al. 2020

CMAR

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Background: Gastric cancer (GC) is a major cancer-related mortality disease. Gambogic acid (GA) has been investigated to inhibit cancer progression. In the present study, the molecular mechanism of GA in regulating GC progression was studied. Methods: The expression levels of circular RNA ASAP2 (circ_ASAP2), miR-33a-5p and cyclin-dependent kinases 7 (CDK7) were detected by quantitative real-time polymerase reaction (qRT-PCR). CDK7 protein level was evaluated by Western blot. Cell colony formation assay, 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, transwell assay and flow cytometry analysis were employed to reveal the functional effects among circ_ASAP2, miR-33a-5p and CDK7 on GA-induced GC progression. Mechanistically, the binding relationship between miR-33a-5p and circ_ASAP2 or CDK7 was predicted with starBase v3.0 online database and verified by dual-luciferase reporter assay. In vivo tumor formation assay was used to explain the impacts of GA treatment on GC growth in vivo. Results: Circ_ASAP2 and CDK7 expression were downregulated in GA-induced GC cells compared with GC cells. MiR-33a-5p expression was upregulated in GA-induced GC cells relative to GC cells. The protein expression level of CDK7 was lower in GA-induced GC cells than that in GC cells. Further, circ_ASAP2 overexpression decreased GA-induced inhibition effects on cell proliferation, migration and invasion and GA-induced promotion effect on cell apoptosis in both AGS and HGC-27 cells, whereas this phenomenon was reversed by miR-33a-5p. In addition, circ_ASAP2 functioned as a sponge of miR-33a-5p and miR-33a-5p was associated with CDK7. Furthermore, GA treatment inhibited GC growth in vivo. Conclusion: Circ_ASAP2 overexpression promoted cell proliferation, migration and invasion, whereas inhibited cell apoptosis by upregulating CDK7 expression through binding to miR-33a-5p in GA-induced GC cells. This study provided a theoretical basis in GC treatment with GA.

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Circ_0006332 promotes growth and progression of bladder cancer by modulating MYBL2 expression via miR-143

Cited by 19 publications

References 36 publications

lncRNA RPSAP52 induced the development of tongue squamous cell carcinomas via miR‐423‐5p/MYBL2

lncRNA RPSAP52 induced the development of tongue squamous cell carcinomas via miR‐423‐5p/MYBL2

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

<p>Gambogic Acid Inhibits the Progression of Gastric Cancer via circRNA_ASAP2/miR-33a-5p/CDK7 Axis</p>

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