LncRNA CALML3-AS1 promotes tumorigenesis of bladder cancer via regulating ZBTB2 by suppression of microRNA-4316

Wang, Feng; Zu, Yanwen; Huang, Weijian; Chen, Hongde; Xie, Hui; Yu, Yang

doi:10.1016/j.bbrc.2018.08.150

Cited by 33 publications

(34 citation statements)

References 24 publications

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“…Through browsing TargetScan (http://www.targetscan.org/vert_72/), we found that ZBTB2 was a putative target for miR‐488‐3p. ZBTB2 is a newly discovered gene which has been reported to act as an oncogene in several cancers, so we chose ZBTB2 for further investigation. Results of qPCR confirmed the elevation of ZBTB2 expression in ESCC tissues, and IHC analysis also revealed that ZBTB2 showed higher positivity in ESCC tissues in contrast to the matched normal tissues (Figure A).…”

Section: Resultsmentioning

confidence: 99%

MicroRNA‐488‐3p inhibits proliferation and induces apoptosis by targeting ZBTB2 in esophageal squamous cell carcinoma

Yang

et al. 2019

J of Cellular Biochemistry

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Esophageal squamous cell carcinoma (ESCC) is the eighth most prevalent cancer and the sixth leading cause for cancer‐associated mortality. MicroRNAs (miRNAs) are increasingly reported to exert important regulatory functions in human cancers by regulating certain gene expression. miR‐488‐3p has been identified to be a tumor suppressor in multiple cancers, but its role in ESCC is yet to be investigated. The present study aimed to uncover the biological role and modulatory mechanism of miR‐488‐3p in ESCC. We first revealed the downregulation of miR‐488‐3p in ESCC tissues and cell lines. Gain‐of‐function assays confirmed that miR‐488‐3p overexpression abrogated proliferation and accelerated apoptosis. Mechanistically, we identified via bioinformatics tool and confirmed that zinc finger and BTB domain containing 2 (ZBTB2) was a target for miR‐488‐3p. Moreover, miR‐488‐3p activated the p53 pathway through suppressing ZBTB2. Finally, rescue assays proved that ZBTB2 was involved in the regulation of miR‐488‐3p on proliferation and apoptosis in ESCC. Additionally, we verified that miR‐488‐3p had alternate targets in ESCC by confirming the involvement of protein kinase, DNA‐activated, catalytic subunit (PRKDC), a known target for miR‐488‐3p, in miR‐488‐3p‐mediated regulation on ESCC. In sum, this study revealed that miR‐488‐3p inhibited proliferation and induced apoptosis by targeting ZBTB2 and activating p53 pathway in esophageal squamous cell carcinoma, providing a novel biological target for ESCC.

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Section: Resultsmentioning

confidence: 99%

MicroRNA‐488‐3p inhibits proliferation and induces apoptosis by targeting ZBTB2 in esophageal squamous cell carcinoma

Yang

et al. 2019

J of Cellular Biochemistry

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“…Additionally, miR-4316 upregulation was able to suppress gastric cancer cells proliferation and migration in vitro. MIR-4316 was reported to inhibit tumor progression in breast cancer, papillary thyroid cancer, bladder cancer, and hepatocellular carcinoma [17][18][19][20]. On the contrary, in early colon cancer, miR-4316 and miR-506 expression were elevated in peripheral blood of early colon cancer [27].…”

Section: Discussionmentioning

confidence: 99%

“…Initially, It was known that both of miR-221 and miR-222 regulate the angiogenic properties of human umbilical vein endothelial cells, overexpression of miR-221 and miR-222 effect p27(Kip1), p57(kip2) and c-kit expression and inhibit endothelial cell-promoted tube formation [16]. Recently, it has been indicated that miR-4316 acts as a tumor suppressor or oncogene in two different cancers [17][18][19][20].…”

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confidence: 99%

MicroRNA-4316 inhibits gastric cancer proliferation and migration via directly targeting VEGF-A

et al. 2020

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Background and aims: microRNAs (miRNAs) have been reported to regulate proliferation and migration by downregulating the expression of target genes. The aims of this study were to investigate whether miR-4316 inhibited proliferation and migration by downregulating vascular endothelial growth factor A (VEGF-A) and its clinical significance in gastric cancer (GC). Methods: The clinical tissues of the GC patients for miR-4316 and VEGF-A were detected by qRT-PCR. The protein levels of VEGF-A and c-Met were determined by western blotting. Cell Proliferation, migration, and colony forming assays were conducted to show whether miR-4316 affects proliferation by CCK-8, migration by transwell, wound healing and colony formation assays. The bioinformatic methods and luciferase reporter assay were applied to detect the relationship between miRNA and VEGF-A on its targeting 3-untranslated regions (3-UTRs). CCK-8, colony formation, wound healing, and transwell assay were performed to explore the function of miR-4316. Results: The results of qRT-PCR indicated that miR-4316 expression level was significantly downregulated in human GC tissues and GC cell lines compared with their control. miR-4316 inhibited proliferation, migration and colony formation in GC cell lines by reducing VEGF-A. And western blot results indicated that miR-4316 significantly inhibited GC through repressing VEGF-A and c-Met. The investigation of Luciferase assay indicated that VEGF-A is a direct target gene of miR-4316. Conclusions: miR-4316 suppressed proliferation and migration of GC through the VEGF-A gene. MiR-4316 acts as a tumor suppressor by targeting VEGF-A and this indicated that MiR-4316 might be a potential therapeutic target for GC.

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“…For example, lncRNA ROCR suppressed endogenous cardiac regeneration by targeting the PTEN/Akt pathway . LncRNA CALML3‐AS1 promotes tumorigenesis of bladder cancer via regulating ZBTB2 by suppression of miR‐4316 . However, the relationship between lncRNA and myocardial infarction remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

“…16 LncRNA CALML3-AS1 promotes tumorigenesis of bladder cancer via regulating ZBTB2 by suppression of miR-4316. 17 However, the relationship between lncRNA and myocardial infarction remains largely unknown. Thus, there is no doubt that exploring new lncRNA and intervention target will shed new light on clinical treatment.…”

mentioning

confidence: 99%

Overexpression of lncRNA Gm2691 attenuates apoptosis and inflammatory response after myocardial infarction through PI3K/Akt signaling pathway

Tian

et al. 2019

IUBMB Life

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Acute myocardial infarction is one of the most threatening disease in the world. In previous studies, numerous dysregulated lncRNAs exposed to ischemic reperfusion injury have been identified. In this differential lncRNAs, Gm2691 attracted our attention due to its high fold change. The aim of the study was to investigate the function and mechanism of lncRNA Gm2691 in ischemic reperfusion injury. AnaeroPack anaerobic system treated neonatal rat ventricular cardiomyocytes were used to analyze the function of lncRNA Gm2691 in vitro. Tunel, Caspase3, and inflammation markers were detected to evaluate apoptosis and inflammatory response. Rat acute myocardial infarction was performed to elucidate the function of lncRNA Gm2691 in vivo. The results showed that LncRNA Gm2691 improved the cardiac function and attenuated the inflammatory response in vivo. We also found that lncRNA Gm2691 reduced the apoptosis and improved cell survival rates in anaeroPack anaerobic system treated neonatal rat ventricular cardiomyocytes. Western blot analysis revealed that lncRNA Gm2691 decreased Akt and ERK1/2 activities, suggesting that lncRNA Gm2691 may functioned through Akt signaling pathway. We verified the function and mechanism of lncRNA Gm2691 and provide evidence that lncRNA Gm2691 may play important role in ischemic reperfusion injury, and understanding the precise role of Gm2691 will undoubtedly shed new light on the clinical treatment.

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LncRNA CALML3-AS1 promotes tumorigenesis of bladder cancer via regulating ZBTB2 by suppression of microRNA-4316

Cited by 33 publications

References 24 publications

MicroRNA‐488‐3p inhibits proliferation and induces apoptosis by targeting ZBTB2 in esophageal squamous cell carcinoma

MicroRNA‐488‐3p inhibits proliferation and induces apoptosis by targeting ZBTB2 in esophageal squamous cell carcinoma

MicroRNA-4316 inhibits gastric cancer proliferation and migration via directly targeting VEGF-A

Overexpression of lncRNA Gm2691 attenuates apoptosis and inflammatory response after myocardial infarction through PI3K/Akt signaling pathway

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