circCELSR1 facilitates ovarian cancer proliferation and metastasis by sponging miR-598 to activate BRD4 signals

Zeng, Xiangyang; Yuan, Jing; Wang, Chen; Zeng, Da; Yong, Jiahui; Jiang, Xingming; Lan, Hua; Xiao, Songshu

doi:10.1186/s10020-020-00194-y

Cited by 24 publications

(11 citation statements)

References 39 publications

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“…Previous study confirmed that BRD4, whose effect was found up-regulated in PA, could regulate the growth of PA tumor in mice [ 30 , 31 ], and therefore, we chose BRD4 for further analysis in the current study. BRD4 has been widely reported to be involved in the development of various cancer types, including multiple myeloma [ 32 ], small cell lung cancer [ 33 ], and ovrican cancer [ 34 ]. The expression of BRD4 could notably affect multiple biological characteristics via different approaches.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA PCAT6 regulates the progression of pituitary adenomas by regulating the miR-139-3p/BRD4 axis

Zhao

Cheng

et al. 2021

Cancer Cell Int

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Background Dysregulated lncRNA PCAT6 was discovered in many cancers excluding pituitary adenomas (PA). Therefore, we explored the role of PCAT6 in PA in this research. Methods Abnormally expressed miRNAs were analyzed by bioinformatics and RT-qPCR. The target and regulator of miR-139-3p were determined by bioinformatics, dual-luciferase reporter assay, or RIP. The correlation among PCAT6, miR-139-3p, and BRD4 was further analyzed. The viability, apoptosis, cell cycle distribution of PA cells, as well as their ability to invade, migrate, and proliferate, were tested after transfection through CCK-8, flow cytometry, transwell, wound healing, and colony formation assays. After construction of transplanted-tumor model in nude mice, cell apoptosis in the tumor was detected by TUNEL. The expressions of PCAT6, BRD4, miR-139-3p, and apoptosis-related factors in PA tissues, cells, or tumor tissues were detected by RT-qPCR, Western blot, or IHC. Results PCAT6 and BRD4 were high-expressed but miR-139-3p was low-expressed in PA. Both the 3′-untranslated regions of PCAT6 and BRD4 mRNAs were demonstrated to contain a potential binding site for miR-139-3p. PCAT6 was positively correlated to BRD4, and miR-139-3p was negatively correlated to PCAT6 and BRD4. MiR-139-3p mimic, shPCAT6 and siBRD4 inhibited the viability, migration, invasion, and proliferation of PA cells while inducing apoptosis. MiR-139-3p mimic and shPCAT6 inhibited the cell cycle progression of PA cells, decreased the weight and volume of the xenotransplanted tumor, and reduced the levels of Bcl-2 and BRD4 while enhancing the levels of Bax, miR-139-3p, and Cleaved caspase-3. MiR-139-3p inhibitor caused the opposite effect of miR-139-3p mimic and further reversed the effect of shPCAT6 on on PA cells. Conclusion PCAT6 regulated the progression of PA via modulating the miR-139-3p/BRD4 axis, which might provide a novel biomarker for the prevention, diagnosis, and treatment of PA.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA PCAT6 regulates the progression of pituitary adenomas by regulating the miR-139-3p/BRD4 axis

Zhao

Cheng

et al. 2021

Cancer Cell Int

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“…There is evidence that one of the mechanisms of circRNA is to act as a sponge of microRNA (miRNA) to mediate downstream targeted mRNA expression. 15 In many studies, miR-598 has been identified as a tumor suppressor mediating the regulation of cancer progression, such as in ovarian cancer 16 and gastric cancer. 17 In NSCLC, miR-598 expression has been found to be significantly low and associated with the malignant progression of NSCLC.…”

Section: Introductionmentioning

confidence: 99%

Circ_0007580 knockdown strengthens the radiosensitivity of non‐small cell lung cancer via the miR‐598‐dependent regulation of THBS2

Yang

Zhang

et al. 2022

Thoracic Cancer

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Background: Radioresistance is a common cause of treatment failure in many cancers, including non-small cell lung cancer (NSCLC). Circular RNA (circRNA) has been shown to be involved in the radiosensitivity of many cancers. However, the role and mechanism of circ_0007580 in the radiosensitivity of NSCLC remain unclear. Methods: The expression levels of circ_0007580, miR-598 and thrombospondin 2 (THBS2) were estimated by quantitative real-time PCR. The radiosensitivity of cells was measured using colony formation assay. Cell proliferation and apoptosis were assessed by performing cell counting kit 8 assay, colony formation assay, flow cytometry, and by detecting caspase-3 and caspase-9 activities. Protein expression was determined using western blot analysis. Results: Our data showed that circ_0007580 was highly expressed and miR-598 was lowly expressed in radioresistant NSCLC tissues. Functional experiments suggested that circ_0007580 silencing could improve the radiosensitivity of cells by suppressing cell proliferation and increasing apoptosis. MiR-598 was confirmed to be a target of circ_0007580, and its inhibitor could reverse the regulation of circ_0007580 on the radiosensitivity of NSCLC cells. MiR-598 was found to target THBS2. The suppressive effect of miR-598 on the radiosensitivity of cells could be reversed by THBS2 overexpression. Additionally, circ_0007580 could sponge miR-598 to regulate THBS2. In vivo experiments showed that knockdown of circ_0007580 enhanced the radiosensitivity of NSCLC tumors. Conclusions: Our results revealed that circ_0007580 might be a target for improving the radiosensitivity of NSCLC, which was mainly achieved by regulating the miR-598/ THBS2 axis.

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“…In some studies, the expression of mirR-598 has been down-regulated in tissue and cells of gastric cancer, and miR-598 over-expresses can inhibit and promote gastric cancer proliferation and metastasis and apoptosis (23,24). Zeng et al (25) found that miR-598 expression in ovarian cancer cells is downregulated and miR-598 inhibition could reverse the circCELSR1 down-regulation on ovarian cancer cell proliferation and metastasis and promote apoptosis. The findings of this study demonstrated that miR-598 was downregulated with Zeng and Liu-like, stomach cancer tissues and cells.…”

Section: Discussionmentioning

confidence: 99%

CircB3GNTL1 and miR-598 regulation effects on proliferation, apoptosis, and glutaminolysis in gastric cancer cells

Yue

Wang

et al. 2020

Cell Mol Biol (Noisy-le-grand)

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This study was performed to research circB3GNTL1 control, miR-598 and its mechanism for cell proliferation, apoptosis and glutamine breakdown.For this purpose, CirB3GNTL1 and miR-598 expressions were detected by qRT-PCR in gastric and cell lines; MTT tests were performed to detect proliferation; flow cytometry was established in flow; glutamine decomposition was evaluated with glutamine, glutamic acid and α-keto-glutaric acid (α-KG) expression; Bcl-2, PCNA, ASCT2 and GLS1 expression levels were calculated; Methods of expression were calculated. The results showed that CircB3GNTL1 expression was up-regulated and miR-598 expression was up-regulated in gastric cancer tissues and cell lines; Knockdown circB3GNTL1 prevented proliferation and glutamine decomposition of the gastric cancer cells and induced apoptosis compared with normal para-cancers and gastric cancer cell lines. Results circB3GNTL1 can target and control miR-598 expression, and miR-598 can reverse the proliferation, apoptosis, and decomposition of glutamine from gastric cancer cells by knockdown circB3GNTL1. It was concluded that CirB3GNTL1 prevents decomposition of glutamines and induces apoptosis by controlling miR-598 in gastric cancer cells.

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circCELSR1 facilitates ovarian cancer proliferation and metastasis by sponging miR-598 to activate BRD4 signals

Cited by 24 publications

References 39 publications

RETRACTED ARTICLE: LncRNA PCAT6 regulates the progression of pituitary adenomas by regulating the miR-139-3p/BRD4 axis

RETRACTED ARTICLE: LncRNA PCAT6 regulates the progression of pituitary adenomas by regulating the miR-139-3p/BRD4 axis

Circ_0007580 knockdown strengthens the radiosensitivity of non‐small cell lung cancer via the miR‐598‐dependent regulation of THBS2

CircB3GNTL1 and miR-598 regulation effects on proliferation, apoptosis, and glutaminolysis in gastric cancer cells

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