<i>Retracted</i>: High expression of TCF12 contributes to gastric cancer development via being target regulated by miR‐183 and activating PI3K/AKT pathway

Wang, Xuekui; Gao, Shen; Xie, Feng; Li, Wei; Li, Miyang; Ning, Yan; Gao, Tiehe; Fang, Ling

doi:10.1002/jcb.28664

Cited by 17 publications

(10 citation statements)

References 34 publications

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“…In hepatocellular carcinoma, overexpression of TCF12 in human HCC cells enhances cell proliferation, migration, and invasion (Yang et al, 2019). In gastric cancer, suppression of TCF12 inhibits proliferation of gastric cancer cells via regulation by miR‐183 (Wang, Gao, et al, 2019). In contrast, in prostate cancer, TCF12 suppresses the proliferation, invasion, and migration of prostate cancer cells (Q.…”

Section: Discussionmentioning

confidence: 99%

circHIPK3 regulates proliferation and differentiation of myoblast through the miR‐7/TCF12 pathway

Gao

Yang

et al. 2021

Journal Cellular Physiology

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Skeletal muscle development is a complex biological process involving multiple key genes, signaling pathways and noncoding RNAs, including microRNAs and circular RNAs (circRNAs). However, the regulatory relationship among them is so complicated that it has not yet been fully elucidated. In this study, we found that miR‐7 inhibited C2C12 cell proliferation and differentiation by targeting transcription factor 12 (TCF12). circHIPK3 acted as a competing endogenous RNA, and its overexpression effectively reversed the regulation of miR‐7 on C2C12 cell proliferation and differentiation by increasing TCF12 expression. Taken together, our findings provide evidence that circHIPK3 regulates skeletal muscle development through the miR‐7/TCF12 pathway. This study provides a scientific basis for further research on skeletal muscle development at the circRNA level.

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Section: Discussionmentioning

confidence: 99%

circHIPK3 regulates proliferation and differentiation of myoblast through the miR‐7/TCF12 pathway

Gao

Yang

et al. 2021

Journal Cellular Physiology

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“…13 Increasing studies have shown that TCF12 acts as an oncogene/a tumor suppressor in a variety of human cancers. 14 For instance, TCF-12 is a potential molecular target that inhibits the invasion and metastasis of gallbladder cancer cells. 15 TCF12 is significantly elevated in cancer-related fibroblasts, causing extracellular matrix remodeling and triggering invasion and metastasis of breast cancer cells in vitro and in vivo.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA EMX2OS, Regulated by TCF12, Interacts with FUS to Regulate the Proliferation, Migration and Invasion of Prostate Cancer Cells Through the cGMP-PKG Signaling Pathway</p>

Wang¹,

Zhang²,

Chang³

et al. 2020

OTT

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Background LncRNA EMX2OS (EMX2 opposite strand/antisense RNA) is notably downregulated in prostate cancer (PCa) tissues and may be regarded as a potential molecular biomarker for diagnosis and prognosis. However, its exact role in regulating the development of PCa is obscure. Methods The EMX2OS expression was assessed in PCa tissues, paracancer tissues, PCa cells and normal prostate epithelial cells by qPCR. Gain- and loss-of-function experiments were performed to investigate the role of EMX2OS and FUS in cGMP-PKG (cyclic guanosine monophosphate-dependent protein kinase)-mediated proliferation, invasion, and migration in human PCa cell lines DU145 and PC3. Then, the interaction of transcription factor 12 (TCF12) with EMX2OS promoter was confirmed by using the dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays. RNA binding protein immunoprecipitation and RNA pull-down assays were used to verify the interaction between EMX2OS and FUS protein. Finally, the role of EMX2OS and FUS in tumor growth in vivo was validated in a xenograft nude mouse model. Results TCF12 and EMX2OS were both downregulated in PCa tissues and cells, and they negatively regulated cell proliferation, migration and invasion, and activated cGMP-PKG pathway in DU145 and PC3 cells. TCF12 was a transcription factor of EMX2OS. TCF12 and EMX2OS overexpression both down-regulated cell proliferation, migration and invasion, and activated cGMP-PKG pathway in DU145 and PC3 cells. Furthermore, EMX2OS directly bound with FUS protein and had a synergy effect with FUS protein on cGMP-PKG-mediated cell functions, which could be suppressed by (D)-DT-2 (a cGMP-PKG inhibitor). In addition, the overexpression of FUS or EMX2OS individually markedly decreased the volume and weight of tumors in vivo, and co-overexpression of them further inhibited tumor growth. Conclusion EMX2OS, transcriptionally regulated by TCF12, played a synergy role with FUS protein in regulating the proliferation, migration and invasion of PCa cells by activating the cGMP-PKG pathway.

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“…RT-qPCR and western blot showed that Nur77 knock-out could effectively reduce the expression of CXCR4 and PI3K in U257 and U87 cells. CXCR4 is a key factor mediating PI3K activation [26], which is critical for the activation of the biologi-cal activity of tumour cells [27][28][29][30]. In this study, cellular immunofluorescence assay showed that Nur77 knock-out significantly reduces the nuclear entry of PI3K protein, which may be the main factor leading to the decrease in biological activity of U257 and U87 cells.…”

Section: Discussionmentioning

confidence: 58%

Nur77 knock-down suppresses glioma by regulating CXCR4

et al. 2020

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IntroductionThe aim of this study is to explain the effects and mechanisms of Nur77 in glioma development.Material and methodsNur77 protein and gene expression were measured by immunohistochemistry and real-time quantitative polymerase chain reaction (RT-qPCR) in tissues from glioma and craniocerebral injury patients. The patients were divided into two groups according to median Nur77 gene expression and the correlations between clinical pathology, progression-free survival (PFS), overall survival (OS), and Nur77 gene expression were analysed. U257 and U87 cells were employed to assess the effects of Nur77 in cancer cell development by MTT, flow cytometry, and transwell and wound healing assays. Relative protein and gene expression were evaluated by Western blot assay and RT-qPCR, and PI3K nuclear volumes were evaluated by cellular immunofluorescence to explain the relevant mechanisms.ResultsCompared with that in normal tissues, Nur77 protein and gene expression in glioma tissues was significantly up-regulated (p < 0.01); this up-regulation increased with increasing tumour stage (p < 0.01). Compared with the high Nur77 expression group, the low Nur expression group showed significantly improved PFS and OS (both p < 0.01). Nur77 gene expression appeared to be closely correlated with clinical pathology. In vitro studies of si-Nur77 transfection revealed a significant reduction in the cell viability of the si-Nur77 group, with increasing apoptosis rate (p < 0.001). Nur77 knock-down resulted in significant downregulation of cell invasion and wound healing rates in the si-Nur77 group (p < 0.01), with remarkable reductions in CXCR4 and PI3K.ConclusionsNur77 is an important oncogene in glioma, and Nur77 expression is closely correlated with glioma clinical pathology, PFS, and OS. Nur77 knock-down exerts inhibitory effects on glioma by regulating CXCR4/PI3K.

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Retracted: High expression of TCF12 contributes to gastric cancer development via being target regulated by miR‐183 and activating PI3K/AKT pathway

Cited by 17 publications

References 34 publications

circHIPK3 regulates proliferation and differentiation of myoblast through the miR‐7/TCF12 pathway

circHIPK3 regulates proliferation and differentiation of myoblast through the miR‐7/TCF12 pathway

<p>LncRNA EMX2OS, Regulated by TCF12, Interacts with FUS to Regulate the Proliferation, Migration and Invasion of Prostate Cancer Cells Through the cGMP-PKG Signaling Pathway</p>

Nur77 knock-down suppresses glioma by regulating CXCR4

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