RETRACTED: miR‐212/132 downregulates <scp>SMAD2</scp> expression to suppress the <scp>G1/S</scp> phase transition of the cell cycle and the epithelial to mesenchymal transition in cervical cancer cells

Zhao, Jianli; Zhang, Le; Guo, Xu; Wang, Jinghua; Zhou, Wen; Liu, Min; Li, Xin; Tang, Hua

doi:10.1002/iub.1381

Cited by 71 publications

(59 citation statements)

References 35 publications

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“…Smurf2, an ubiquitin ligase for Smads, also plays a vital role in the adjustment of TGF-β1/Smad signaling [40]. Smad was found to be negatively regulated by overexpression of miRNA [41]. As reflected in our study, miR-485 overexpression effectively inhibited the expression levels of Smurf2, α-SMA, TGF-β1 and Smad3.…”

Section: Discussionsupporting

confidence: 48%

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Chronic respiratory conditions continue to plague millions of people worldwide. We aimed to elucidate the detailed mechanisms of microRNA-485 (miR-485) in airway smooth muscle cell (ASMC) proliferation and apoptosis in chronic asthmatic mice. Methods: A mouse model of chronic asthma was established. Ovalbumin was used to induce chronic asthma in the mice. The levels of transforming growth factor β (TGF-β), interleukin (IL)-4, IL-5, IL-13 and IL-17 in bronchoalveolar lavage fluid in mice were measured by enzyme-linked immunoassays (ELISAs). ASMCs were transfected with miR-485 mimic, miR-485 inhibitor and siRNA-Smurf2. The reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analyses were applied to detect the mRNA and protein levels of Smurf2, α-SMA, TGF-β1 and decapentaplegic homolog (Smads). The MTT assay was utilized for cell proliferation, while flow cytometry was conducted to assess cell cycle distribution and apoptosis. Results: Lower expression of miR-485 and higher expression levels of TGF-β1, IL-4, IL-5, IL-13 and IL-17 were detected in mice with chronic asthma. Smurf2 was identified as the target gene of miR-485. Upregulation of miR-485 mimic and downregulation of Smurf2 decreased expression levels of Smurf2, α-SMA, TGF-β1 and Smad3, inhibited cell proliferation and increased apoptosis, while contrary results were observed in ASMCs transfected with miR-485 inhibitor. Conclusion: Overexpressed miR-485 inhibits cell proliferation and promotes apoptosis of ASMCs through the Smurf2-mediated TGF-β/Smads signaling pathway in mice with chronic asthma.

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Section: Discussionsupporting

confidence: 48%

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

Wang

et al. 2018

Cell Physiol Biochem

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“…miR-132 is located on human chromosome 17p13.3, which is associated with various types of human cancer including osteosarcoma, gastric cancer (21), colorectal cancer (22), prostate cancer (23), breast cancer (24,25), hepatocellular carcinoma (26), pancreatic cancer (27,28) and glioma (29). Zhao et al (14) reported that the expression levels of miR-132 in CC tissues were lower compared with those in adjacent non-cancerous tissues, and it was revealed that miR-132 downregulated SMAD family member (SMAD)2 expression in order to suppress the G1/S phase transition of the cell cycle and the epithelial to mesenchymal transition (EMT) in CC cells. However, the mechanism resulting in the low expression of miR-132 in CC remains largely unknown.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, TSLP produced by CC cells promotes angiogenesis in an EOS-dependent and -independent manner (10,11). Watanabe et al (12) reported that high (14) reported that miR-132 expression was decreased in CC tissues compared with that in adjacent non-cancerous tissues. Transforming growth factor (TGF)-β is a multifunctional cytokine and may induce numerous important signaling pathways in several types of cancer cells (15,16).…”

Section: Introductionmentioning

confidence: 99%

Human thymic stromal lymphopoietin promotes the proliferation and invasion of cervical cancer cells by downregulating microRNA‑132 expression

et al. 2017

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Abstract. Thymic stromal lymphopoietin (TSLP), produced by cervical cancer (CC) cells, promotes angiogenesis, and the recruitment and functional regulation of eosinophils. It has been reported that microRNA (miR)-132 is aberrantly decreased in CC tissues. However, the function and mechanism of TSLP on the biological behaviors of CC cells is largely unknown. The aim of the present study was to investigate the effect of TSLP on the expression of miR-132 and the proliferation and invasion in vitro of CC cell lines, namely, HeLa and SiHa cells. The transcrpitional level of miR-132 was analyzed using reverse transcription-quantitative polymerase chaon reaction. The proliferation, invasion, and the expression of proliferation and invasion-related molecules in HeLa and SiHa cells in vitro were evaluated using bromodeoxyuridine cell proliferation, Matrigel invasion assays, flow cytometry and ELISA, respectively. Here, it was revealed that recombinant human TSLP (rhTSLP) downregulated the expression levels of miR-132 in HeLa and SiHa cells, and by contrast, the neutralizing antibodies for TSLP or TSLP receptor (TSLPR) upregulated miR-132 expression levels in HeLa and SiHa cells. The overexpression of miR-132 resulted in a lowered proliferation and invasiveness, decreased levels of proliferation-associated molecules marker of proliferation Ki-67 and proliferating cell nuclear antigen, and the decreased production of matrix metalloproteinase (MMP)2 and MMP9 in HeLa and SiHa cells. Compared with the control group, there was a higher level of proliferation and invasion in HeLa and SiHa cells following stimulation with rhTSLP. However, these effects induced by rhTSLP were significantly impaired in HeLa and SiHa cells with miR-132 overexpression. The results of the present study indicated that TSLP produced by CC cells downregulated miR-132 expression, and stimulated the proliferation and invasion of CC cells, thereby further promoting the development of CC. IntroductionCervical cancer (CC) is one of the most common gynecological malignancies with high rates of morbidity (0.001-0.05%) and mortality (0.0024-0.0175%), endangering the health and quality of life of women globally (1). Although the decreased incidence of CC has primarily been attributed to the widespread use of cytological screening, invasive CC remains an issue regarding the mortality rates of patients with CC. Thus, the elucidation of the molecular pathogenesis of CC is urgently required. The pathogenesis of CC remains enigmatic and may be connected with numerous factors, including infection with high-risk human papillomaviruses (HPVs) (2).Thymic stromal lymphopoietin (TSLP) is primarily produced by stromal cells, epithelial cells, fibroblasts, keratinocytes, basophils and other types of cells, including mast cells, smooth muscle cells, fibroblasts, dendritic cells, trophoblasts, and cancer or cancer-associated cells (3-5). TSLP may trigger helper T-cell 2 cytokines, and is associated with airway inflammatory disease, immunoglobulin E production, allergic respons...

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“…For the immunofluorescence assay, cells were incubated with anti-CADM2 antibody (1:100) and viewed using fluorescence microscopy. This assay was performed according to the method described by Zhao et al [48].…”

Section: Immunohistochemical Staining and Immunofluorescencementioning

confidence: 99%

Hypoxia-Regulated miR-146a Targets Cell Adhesion Molecule 2 to Promote Proliferation, Migration, and Invasion of Clear Cell Renal Cell Carcinoma

Yang¹,

Zhao²,

Wang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: miR-146a has recently been shown to promote cell proliferation, migration, and invasion in many cancers, but the role of miR-146a in clear cell renal cell carcinoma (ccRCC) remains unclear. Methods: Reverse transcription quantitative PCR (RT-qPCR) was performed to investigate the mRNA expression of miR-146a and CADM2 in ccRCC tissues. The luciferase reporter assay, Western blotting, and ChIP assay were carried out to explore the promoter and the transcription factor of miR-146a. Moreover, the effect of miR-146a and CADM2 on ccRCC cells was explored using methyl thiazolyl tetrazolium, colony formation, and migration and invasion assays. The luciferase reporter assay, RT-qPCR, western blotting, and immunofluorescence assay were carried out to investigate whether CADM2 is directly regulated by miR-146a. A tumor xenograft model and immunohistochemical staining were used to examine the carcinogenic effect of miR-146a and CADM2 in vivo. Results: miR-146a has been shown to promote cell proliferation, migration, and invasion. Here, we found that miR-146a is highly expressed in ccRCC tissues, whereas CADM2 is down-regulated. Hypoxia can induce the expression of miR-146a by stimulating its promoter. In addition, we demonstrated that miR-146a promoted and CADM2 inhibited proliferation, migration, and invasion of ccRCC cells. The 3’ untranslated region (UTR) luciferase reporter assay identified that miR-146a targeted the 3’ UTR of CADM2 and negatively regulated its expression. Ectopic expression of CADM2 counteracted the promoting effect of miR-146a on cell proliferation, migration, invasion, and the epithelial–mesenchymal transition process. Conclusion: Together, the finding of down-regulation of CADM2 by miR-146a can provide new insights into ccRCC pathogenesis and might contribute to the development of novel therapeutic strategies.

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RETRACTED: miR‐212/132 downregulates SMAD2 expression to suppress the G1/S phase transition of the cell cycle and the epithelial to mesenchymal transition in cervical cancer cells

Cited by 71 publications

References 35 publications

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

Human thymic stromal lymphopoietin promotes the proliferation and invasion of cervical cancer cells by downregulating microRNA‑132 expression

Hypoxia-Regulated miR-146a Targets Cell Adhesion Molecule 2 to Promote Proliferation, Migration, and Invasion of Clear Cell Renal Cell Carcinoma

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