STAT3‐induced upregulation of lncRNA ABHD11‐AS1 promotes tumour progression in papillary thyroid carcinoma by regulating miR‐1301‐3p/STAT3 axis and PI3K/AKT signalling pathway

Jiang, Wen Guo; Wang, Hongwei; Dong, Tingjun; panpan, GAN; Fang, Henghu; Wu, Sudong; Li, Jingjiao; Zhang, Yuanyuan; Du, Rui; Zhu, Qingqing

doi:10.1111/cpr.12569

Cited by 67 publications

(61 citation statements)

References 51 publications

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“…Similarly, NNT-AS1 promoted bladder cancer cell proliferation by targeting miR-1301-3p/PODXL axis and activating Wnt pathway [13] . Besides, ABHD11-AS1 and LINC01433 upregulated STAT3 level by sponging miR-1301-3p and promoted tumor progression in papillary thyroid carcinoma and hepatocellular carcinoma, respectively [14,15] . Hence, the function of miR-1301-3p is needed to elucidate for pancreatic cancer.…”

Section: Discussionmentioning

confidence: 98%

MiR-1301-3p Inhibits Epithelial to Mesenchymal Transition via Targeting RhoA in Pancreatic Cancer

Zhang

et al. 2020

Preprint

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Background: Micro(mi)RNAs play an essential role in the epithelial-mesenchymal transition (EMT) process in human cancers. This study aimed to uncover the regulatory mechanism of miR-1301-3p on EMT in pancreatic cancer (PC).Methods: GEO database (GSE31568, GSE41372, and GSE32688) and the PC cohort of The Cancer Genome Atlas were applied to discover the expression and prognostic role of miR-1301-3p. In the validation cohort, qRT-PCR was performed in 72 paired PC tissue samples. CCK-8, wound healing, and transwell migration assays were used to detect miR-1301-3p function on PC cells. Luciferase reporter assays and western blotting were performed to discover the potential target of miR-1301-3p on EMT.Results: Our study revealed that miR-1301-3p was downregulated in PC tissues compared with normal samples. A low level of miR-1301-3p was associated with malignant pathological differentiation, lymphatic metastasis, tumor residual, and unsatisfactory overall survival. Gene Ontology analyses indicated that miR-1301-3p possibly regulated cell cycle and adheren junction. In vitro assays showed that miR-1301-3p suppressed proliferation, migration, and invasion ability of PC cells. Mechanically, miR-1301-3p inhibits RhoA expression, and knockdown of RhoA upregulated E-cadherin; however, downregulated N-cadherin and vimentin level.Conclusions: MiR-1301-3p acts as a prognostic biomarker for PC and inhibits PC progression by targeting RhoA induced EMT process.

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Section: Discussionmentioning

confidence: 98%

MiR-1301-3p Inhibits Epithelial to Mesenchymal Transition via Targeting RhoA in Pancreatic Cancer

Zhang

et al. 2020

Preprint

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“…In this study, we found that lncRNA MIAT expression was down-regulated after catechin treatment in myocardial Same as the transcriptional regulation of other genes, mounting evidence showed that the transcription of lncRNAs could be regulated by transcription factors at the transcriptional level under physiological and pathological conditions. 36,37 Researchers have found that lncRNA MIAT can be regulated by transcription factor Oct4 in the differentiation of mouse embryonic stem cells. 38 LncRNA MIAT can also be positively regulated by transcription factor c-Myc to promote Müller cell-derived proinflammatory cytokine release.…”

Section: Discussionmentioning

confidence: 99%

Catechin relieves hypoxia/reoxygenation‐induced myocardial cell apoptosis via down‐regulating lncRNA MIAT

Wei

et al. 2020

J Cellular Molecular Medi

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Background Catechin protects heart from myocardial ischaemia/reperfusion (MI/R) injury. However, whether catechin inhibits H/R‐induced myocardial cell apoptosis is largely unknown. Objective This study aims to investigate the underlying mechanism of catechin in inhibiting the apoptosis of H/R‐induced myocardial cells. Methods LncRNA MIAT expression was detected by qRT‐PCR. Cell viability of H9C2 cells was detected using CCK‐8 assay. The apoptosis of H9C2 cells was detected by flow cytometry. The interaction between CREB and MIAT promoter regions was confirmed by dual‐luciferase reporter gene assay and ChIP assay. Results In MI/R rats, catechin improved heart function and down‐regulated lncRNA MIAT expression in myocardial tissue. In H/R‐induced H9C2 cells, catechin protected against cell apoptosis, and lncRNA MIAT overexpression attenuated this protective effect of catechin. We confirmed that transcription factor CREB could bind to MIAT promoter region, and catechin suppressed lncRNA MIAT expression through up‐regulating CREB. Catechin improved mitochondrial function and relieved apoptosis through promoting Akt/Gsk‐3β activation. In addition, MIAT inhibited Akt/Gsk‐3β activation and promoted cell apoptosis in H/R‐induced H9C2 cells. Finally, we found catechin promoted Akt/Gsk‐3β activation through inhibiting MIAT expression in H/R‐induced H9C2 cells. Conclusion Catechin relieved H/R‐induced myocardial cell apoptosis through regulating CREB/lncRNA MIAT/Akt/Gsk‐3β pathway.

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“…LncRNA UCA1 functioned as an endogenous sponge ofmiR-182-5p to positively regulate the expression of Delta-like ligand 4(DLL4) in renal cancer cells (44). In addition, some studies have con rmed that NEAT1 can play a regulatory role through competitively binding different miRNAs in a variety of cancers (45,46). These studies have uncovered a new way to elucidate regulatory mechanisms between NEAT1 and KCTD20.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA NEAT1 regulates glioma cells proliferation and apoptosis by competitively binding with miR-324-5p and upregulating KCTD20 expression

Zhang

Liu

et al. 2020

Preprint

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Background Recent studies have pointed out that long non-coding RNAs (lncRNAs) play a key role in tumorigenesis, including glioma. Nuclear paraspeckle assembly transcript 1 (NEAT1), a lncRNA, has been reported to be participated in the development and progression of many types of tumors and promotes cancer cell proliferation, migration, invasion, and drug resistance. The exact role and regulatory mechanism of NEAT1 in gliomas still need to be further explored. Methods NEAT1 expression was detected in paired glioma tissues and adjacent normal tissues, as well as in glioma cell lines by quantitative real-time PCR (qRT-PCR). Cell viability and apoptosis were measured using flow cytometry, colony formation assays and TdT-mediated dUTP nick-end labeling (TUNEL) assay. The mechanism of competing endogenous RNA (ceRNA) between NEAT1 and miR-324-5p was determined using bioinformatics analysis, RIP and luciferase reporter assay. Results Here we demonstrated that lncRNA NEAT1 was upregulated and significantly associated with poor prognosis in glioma tissues. Through gain- and loss-of NEAT1 expression, we found that knockdown of NEAT1 inhibited the abilities of cell proliferation and induced G0/G1 arrest and apoptosis in vitro, suppressed tumorigenesis in vivo via sponging miR-324-5p and then upregulated KCTD20 expression. In addition, NEAT1 reversed the effects of miR-324-5p on the proliferation and apoptosis of glioma cells, and involved the inhibition of potassium channel tetramerization protein domain containing 20 (KCTD20) expression. Conclusion Collectively, our findings demonstrate that NEAT1 epigenetically up-regulates KCTD20 expression through competitively binding miR-324-5p, and also provides a potential therapeutic target for human glioma.

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STAT3‐induced upregulation of lncRNA ABHD11‐AS1 promotes tumour progression in papillary thyroid carcinoma by regulating miR‐1301‐3p/STAT3 axis and PI3K/AKT signalling pathway

Cited by 67 publications

References 51 publications

MiR-1301-3p Inhibits Epithelial to Mesenchymal Transition via Targeting RhoA in Pancreatic Cancer

MiR-1301-3p Inhibits Epithelial to Mesenchymal Transition via Targeting RhoA in Pancreatic Cancer

Catechin relieves hypoxia/reoxygenation‐induced myocardial cell apoptosis via down‐regulating lncRNA MIAT

Long noncoding RNA NEAT1 regulates glioma cells proliferation and apoptosis by competitively binding with miR-324-5p and upregulating KCTD20 expression

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