Circular RNA hsa_circ_0052112 promotes cell migration and invasion by acting as sponge for miR-125a-5p in breast cancer

Zhang, Heda; Jiang, Linhong; Hou, Jianglong; Zhong, Shanliang; Zhou, Siying; Zhu, Liming; Li, Jian; Wang, Dandan; Sun, Dawei; Ji, Zhenling; Tang, Jinhai

doi:10.1016/j.biopha.2018.08.030

Cited by 77 publications

(71 citation statements)

References 42 publications

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“…FISH assay was carried out as previously described [18]. First of all, 4% formaldehyde was added to incubate with VSMCs for 15 min and then PBS was used to wash them.…”

Section: Fluorescence In Situ Hybridization (Fish) Assaymentioning

confidence: 99%

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3

et al. 2020

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Long noncoding RNAs (lncRNAs) were viewed as crucial participants in the pathogenesis of abdominal aortic aneurysm (AAA). LncRNA NEAT1 was recognized as an oncogenic gene in various diseases. However, its function and mechanism in AAA were not precisely documented. Here, we explored the functional role and molecular mechanism of NEAT1 in AAA. Functionally, the effect of NEAT1 on the proliferation was assessed by CCK-8 and EdU assay, while its impact on the apoptosis was evaluated through caspase-3/9 activity and TUNEL assays. As a result, we found that NEAT1 knockdown enhanced the proliferation and impaired the apoptosis of vascular smooth muscle cells (VSMCs). Reversely, overexpressed NEAT1 exerted anti-proliferation and pro-apoptosis effects in VSMCs. Mechanically, we found that STAT3 acted as a transcription factor and contributed to NEAT1 transcription by ChIP and luciferase reporter assays. In addition, NEAT1 was confirmed as a sponge of miR-4688 and thereby increase the expression of TULP3 in VSMCs via RIP assay and RNA pull-down assay. Rescue experiments indicted that TULP3 overexpressing countervailed the impact of NEAT1 depletion on AAA biological processes. Conclusively, lncRNA NEAT1 induced by STAT3 was identified as a ceRNA and facilitated AAA formation by targeting miR-4688/TULP3 axis.

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“…FISH assay was carried out as previously described [18]. First of all, 4% formaldehyde was added to incubate with VSMCs for 15 min and then PBS was used to wash them.…”

Section: Fluorescence In Situ Hybridization (Fish) Assaymentioning

confidence: 99%

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3

et al. 2020

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“…Xu et al reported that circRNA transcriptional adaptor 2A (circTADA2A) inhibits cell proliferation, migration and invasion by regulating microRNA-203a-3p/suppressor of cytokine signaling 3 (SOCS3) axis in breast cancer [7]. Furthermore, Zhang et al suggested that circRNA has_ circ_0052112, generated from zinc finger 83, could promote cell migration and invasion by sponging microRNA-125a-5p in breast cancer [8]. CircRNA differentially expressed in normal cells and neoplasia domain containing 4C (circDENND4C) is a hypoxiaassociated RNA molecule [9].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of circDENND4C inhibits glycolysis, migration and invasion by up-regulating miR-200b/c in breast cancer under hypoxia

Ren

Liu

Feng

et al. 2019

J Exp Clin Cancer Res

137

105

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Background: Hypoxia is a key feature of breast cancer, which affects cancer development, metastasis and metabolism. Previous studies suggested that circular RNAs (circRNAs) could participate in cancer progression and hypoxia regulation. This study aimed to investigate the role of circRNA differentially expressed in normal cells and neoplasia domain containing 4C (circDENND4C) in breast cancer progression under hypoxia. Methods: Forty-three patients with breast cancer were involved in this study. Breast cancer cell lines MDA-MB-453 and SK-BR-3 were cultured under hypoxia (1% O 2) for experiments in vitro. The expression levels of circDENND4C, microRNA-200b (miR-200b) and miR-200c were measured by quantitative real-time polymerase chain reaction. Glycolysis was investigated by glucose consumption, lactate production and hexokinase II (HK2) protein level. Migration and invasion were evaluated via trans-well assay and protein levels of matrix metallopeptidase 9 (MMP9) and MMP2. The interaction between circDENND4C and miR-200b or miR-200c was explored by bioinformatics analysis, luciferase assay and RNA immunoprecipitation. Murine xenograft model was established to investigate the anti-cancer role of circDENND4C in vivo. Results: circDENND4C highly expressed in breast cancer was up-regulated in response to hypoxia. Knockdown of circDENND4C decreased glycolysis, migration and invasion in breast cancer cells under hypoxia. circDENND4C was validated as a sponge of miR-200b and miR-200c. Deficiency of miR-200b or miR-200c reversed the suppressive effect of circDENND4C knockdown on breast cancer progression. Moreover, silence of circDENND4C reduced xenograft tumor growth by increasing miR-200b and miR-200c. Conclusion: circDENND4C silence suppresses glycolysis, migration and invasion in breast cancer cells under hypoxia by increasing miR-200b and miR-200c.

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“…An increasing number of studies have uncovered that circRNA has contributed a lot to complicated processes of cancer development. For instance, circ‐0052112 accelerates migration and invasion of breast cancer cells by sponging miR‐125a‐5p 17 . circ‐0000467 activates gastric cancer cell proliferation, migration, and invasion acting as a biomarker for gastric cancer 18 .…”

Section: Introductionmentioning

confidence: 99%

Circular RNA (circ‐0075804) promotes the proliferation of retinoblastoma via combining heterogeneous nuclear ribonucleoprotein K (HNRNPK) to improve the stability of E2F transcription factor 3 E2F3

Zhao

Wang

Qin

et al. 2020

J of Cellular Biochemistry

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It is growingly recognized that messenger RNAs (mRNAs) are important regulators of various cancers. However, there are few reporters about the function of E2F3 in retinoblastoma (RB), which needs more exploration. In addition, the circRNA circ-0075804 was derived from the E2F3 host gene. The purpose of the study is to figure out the role and molecular regulation mechanism of E2F3 and circ-0075804 in RB. The role of E2F3 in RB was determined through E2F3 silencing and loss of expression was evaluated by real-time quantitative polymerase chain reaction (RT-qPCR), Western blot, CCK-8, colony formation, and 5-ethynyl-2′-deoxyuridine assays. The interactions between E2F3 and circ-0075804 were validated through loss and gain function of circ-0075804. Besides, the role of circ-0075804 in RB was determined by several functional assays. And the binding ability between heterogeneous nuclear ribonucleoprotein K and circ-0075804 was verified by RNA pull-down, Western blot, and RT-qPCR assays. The expression of E2F3 was upregulated in RB cell lines. Furthermore, knockdown of E2F3 inhibited cell proliferation and induced cell apoptosis in RB. And circ-0075804 positively regulated the expression of E2F3. Moreover, circ-0075804 facilitated cell proliferation and suppressed cell apoptosis. Besides, HNRNPK could bind with circ-0075804 in RB. Finally, knockdown of E2F3 partly rescued the promoting role of circ-0075804 overexpression in RB. Overall, circ-0075804 promotes the proliferation of RB via combining HNRNPK to improve the stability of E2F3, which brings new light for treating RB. K E Y W O R D S circ-0075804, E2F3, HNRNPK, retinoblastoma

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Circular RNA hsa_circ_0052112 promotes cell migration and invasion by acting as sponge for miR-125a-5p in breast cancer

Cited by 77 publications

References 42 publications

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3

STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3

Knockdown of circDENND4C inhibits glycolysis, migration and invasion by up-regulating miR-200b/c in breast cancer under hypoxia

Circular RNA (circ‐0075804) promotes the proliferation of retinoblastoma via combining heterogeneous nuclear ribonucleoprotein K (HNRNPK) to improve the stability of E2F transcription factor 3 E2F3

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