RETRACTED ARTICLE: miR-200a-3p plays tumor suppressor roles in gastric cancer cells by targeting KLF12

Jia, Changhe; Zhang, Yanrui; Xie, Youhua; Ren, Ying; Zhang, Haihui; Zhou, Yicheng; Gao, Ning; Ding, Song‐Ze; Han, Sun‐Young

doi:10.1080/21691401.2019.1594857

Cited by 32 publications

(20 citation statements)

References 20 publications

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“…MicroRNAs (miRNA) have been investigated to participate in the pathological process of many diseases by regulating cell metabolism, proliferation, migration, apoptosis, and drug resistance [ 26 , 27 ]. MiR-200a-3p is a functional miRNA and has been demonstrated to inhibit cell tumorigenesis in many types of cancers, such as papillary thyroid carcinoma [ 28 ], gastric cancer [ 29 ], renal cancer [ 30 ], and so on. In addition, miR-200a-3p also was implied to involve in the regulation of drug resistance.…”

Section: Discussionmentioning

confidence: 99%

Exosomes Mediated Transfer of Circ_UBE2D2 Enhances the Resistance of Breast Cancer to Tamoxifen by Binding to MiR-200a-3p

Liu

et al. 2020

Med Sci Monit

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Background Circular RNA UBE2D2 (circ_UBE2D2) has been found to be involved in the progression of breast cancer. Exosomes are critical mediators of intercellular communication, however, the function of exosomal circ_UBE2D2 in breast cancer remains vague. Material/Methods Cell viability was measured by Cell Counting Kit-8 assay. Western blot was used to detect the levels of estrogen receptor alpha (ERα), E-cadherin, vimentin, CD9, and CD63. Migrated and invaded cells were examined using Transwell assay. Circ_UBE2D2 and microRNA (miR)-200a-3p levels were detected using quantitative real-time polymerase chain reaction. Exosomes were isolated by ultracentrifugation method. The interaction between circ_UBE2D2 and miR-200a-3p was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay. Murine xenograft model was established to conduct in vivo experiments. Results We found that circ_UBE2D2 was upregulated in breast cancer tamoxifen-resistant tissues and cell lines, and circ_UBE2D2 deletion mitigated tamoxifen resistance in breast cancer cells. Circ_UBE2D2 was also significantly loaded in exosomes isolated from resistant cells and could be transferred to parental cells. MiR-200a-3p was a target of circ_UBE2D2, and we demonstrated that exosomes mediated transfer of circ_UBE2D2 interacted with miR-200a-3p to enhance tamoxifen resistance of breast cancer cells by regulating cell viability, metastasis, and the level of ERα in vivo and in vitro . Conclusions Exosomes mediated transfer of circ_UBE2D2 reinforced tamoxifen resistance in breast cancer by binding to miR-200a-3p, providing new insights into the boost of the effectiveness of tamoxifen on breast cancer patients.

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Section: Discussionmentioning

confidence: 99%

Exosomes Mediated Transfer of Circ_UBE2D2 Enhances the Resistance of Breast Cancer to Tamoxifen by Binding to MiR-200a-3p

Liu

et al. 2020

Med Sci Monit

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“…As reported previously, KLF12 was targeted by miR-137 and miR-200a-3p, two tumor suppressor genes in GC. 32 , 33 Furthermore, KLF12 was upregulated in GC, which could participate in lncRNA TTN-AS1 or HOTAIR-mediated GC progression. 34 , 35 Here, we also revealed the upregulation of KLF12 in GC.…”

Section: Discussionmentioning

confidence: 99%

Depletion of Circular RNA circ_CORO1C Suppresses Gastric Cancer Development by Modulating miR-138-5p/KLF12 Axis

Fan¹,

Liu²,

Liu³

et al. 2021

CMAR

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Background: Gastric cancer (GC) is a common and deadly malignancy in the world. CircRNAs have emerged as important regulators in human diseases, including GC. In this work, we intended to explore the role of circ_CORO1C in GC progression and potential mechanism. Methods: Quantitative real-time PCR (qRT-PCR) or Western blot assay was performed to examine the expression of circRNA coronin-like actin-binding protein 1C (circ_CORO1C), microRNA (miR)-138-5p and Krueppel-like factor 12 (KLF12) in clinical samples and cells. Cell colony formation ability and viability were measured by colony formation assay and methyl thiazolyl tetrazolium (MTT) assay, respectively. Expression of cell proliferation and epithelia-mesenchymal transition (EMT) biomarker was detected by Western blot analysis. And cell metastasis, including migration and invasion, and apoptosis were analyzed via Transwell assay and flow cytometry, respectively. Target relationship among circ_CORO1C, miR-138-5p and KLF12 was validated by dual-luciferase reporter assay. The in vivo role of circ_CORO1C was investigated by tumor xenograft assay. Results: Circ_CORO1C and KLF12 were upregulated, while miR-138-5p was downregulated in GC tissues and cells. Circ_CORO1C knockdown suppressed colony formation ability, viability, migration, invasion and EMT in GC cells, while promoted cell apoptosis in vitro. Circ_CORO1C targeted miR-138-5p, the inhibition of which could attenuate silenced circ_CORO1C-induced inhibitory effects on GC progression. MiR-138-5p repressed the aggressive malignant behaviors of GC cells by directly targeting KLF12. Circ_CORO1C deficiency inhibited GC tumor growth in vivo. Conclusion: Depletion of circ_CORO1C suppressed GC progression by regulating miR-138-5p/KLF12 axis, offering a potential molecular target for GC therapy.

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“…In human hepatocellular carcinoma (HCC), the circ-ZEB1.33-miR-200a-3p-CDK6 regulatory axis can regulate HCC cell proliferation [25]. In gastric cancer (GC) tissues, miR-200a-3p plays a cancer suppressing role in GC by targeting KLF12 [26]. In renal cell carcinoma (RCC), the miR-200a-3p/CBL regulatory axis is a new mechanism under pathogenesis [27].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Profiling Reveals an Abundant miR-200a-3p Promotes Skeletal Muscle Satellite Cell Development by Targeting TGF-β2 and Regulating the TGF-β2/SMAD Signaling Pathway

Yin

Shen

et al. 2020

IJMS

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MicroRNAs (miRNAs) are evolutionarily conserved, small noncoding RNAs that play critical post-transcriptional regulatory roles in skeletal muscle development. Chicken is an optimal model to study skeletal muscle formation because its developmental anatomy is similar to that of mammals. In this study, we identified potential miRNAs in the breast muscle of broilers and layers at embryonic day 10 (E10), E13, E16, and E19. We detected 1836 miRNAs, 233 of which were differentially expressed between broilers and layers. In particular, miRNA-200a-3p was significantly more highly expressed in broilers than layers at three time points. In vitro experiments showed that miR-200a-3p accelerated differentiation and proliferation of chicken skeletal muscle satellite cells (SMSCs) and inhibited SMSCs apoptosis. The transforming growth factor 2 (TGF-β2) was identified as a target gene of miR-200a-3p, and which turned out to inhibit differentiation and proliferation, and promote apoptosis of SMSCs. Exogenous TGF-β2 increased the abundances of phosphorylated SMAD2 and SMAD3 proteins, and a miR-200a-3p mimic weakened this effect. The TGF-β2 inhibitor treatment reduced the promotional and inhibitory effects of miR-200a-3p on SMSC differentiation and apoptosis, respectively. Our results indicate that miRNAs are abundantly expressed during embryonic skeletal muscle development, and that miR-200a-3p promotes SMSC development by targeting TGF-β2 and regulating the TGF-β2/SMAD signaling pathway.

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RETRACTED ARTICLE: miR-200a-3p plays tumor suppressor roles in gastric cancer cells by targeting KLF12

Abstract: View related articles View Crossmark data Citing articles: 4 View citing articles miR-200a-3p plays tumor suppressor roles in gastric cancer cells by targeting KLF12

Cited by 32 publications

References 20 publications

Exosomes Mediated Transfer of Circ_UBE2D2 Enhances the Resistance of Breast Cancer to Tamoxifen by Binding to MiR-200a-3p

Exosomes Mediated Transfer of Circ_UBE2D2 Enhances the Resistance of Breast Cancer to Tamoxifen by Binding to MiR-200a-3p

Depletion of Circular RNA circ_CORO1C Suppresses Gastric Cancer Development by Modulating miR-138-5p/KLF12 Axis

MicroRNA Profiling Reveals an Abundant miR-200a-3p Promotes Skeletal Muscle Satellite Cell Development by Targeting TGF-β2 and Regulating the TGF-β2/SMAD Signaling Pathway

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