Long non-coding RNA XIST promotes TGF-β-induced epithelial-mesenchymal transition by regulating miR-367/141-ZEB2 axis in non-small-cell lung cancer

Li, Chang; Liang, Wan; Liu, Zeyi; Xu, Guohai; Wang, Shengjie; Su, Zhiyue; Zhang, Yingxi; Zhang, Cuijuan; Liu, Xia; Li, Zhe; Zhang, Hongtao

doi:10.1016/j.canlet.2018.01.036

Cited by 155 publications

(123 citation statements)

References 51 publications

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“…miR‐367‐3p is involved in regulating a wide range of biological functions and participates in the disease progression of various cancers . Multiple forms of evidence have suggested that miR‐367‐3p expression is downregulated in various cancers, and the overexpression of miR‐367‐3p restricts tumour growth and metastasis . These findings suggest a tumour suppressive function of miR‐367‐3p.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐367‐3p overexpression represses the proliferation and invasion of cervical cancer cells through downregulation of SPAG5‐mediated Wnt/β‐catenin signalling

Yang

Tian

Wang

et al. 2020

Clin Exp Pharma Physio

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MicroRNA‐367‐3p (miR‐367‐3p) has been previously reported as a cancer‐related miRNA that is dysregulated in various cancer types and functions either as an oncogenic or as tumour suppressive miRNA. However, whether miR‐367‐3p is dysregulated in cervical cancer and, further, whether it contributes to the development and progression of the disease remains unknown. Here, our results demonstrated that miR‐367‐3p expression was markedly decreased in both cervical cancer tissues and cell lines compared with corresponding controls. In vitro experiments revealed that miR‐367‐3p overexpression repressed the proliferation and invasion of cervical cancer cells. Notably, sperm‐associated antigen 5 (SPAG5) was identified as a target gene of miR‐367‐3p. Moreover, decreased expression of miR‐367‐3p was correlated with high expression of SPAG5 in cervical cancer tissue specimens. SPAG5 inhibition or miR‐367‐3p overexpression significantly downregulated Wnt/β‐catenin signalling in cervical cancer cells. However, the antitumour effect mediated by miR‐367‐3p overexpression was partially reversed by SPAG5 overexpression. Overall, these findings demonstrate that miR‐367‐3p overexpression restricts the proliferation and invasion of cervical cancer cells through targeting SPAG5 to downregulate Wnt/β‐catenin signalling, suggesting a mechanism for the tumour suppressive function of miR‐367‐3p in cervical cancer. Our study highlights the involvement of miR‐367‐3p/SPAG5/Wnt/β‐catenin signalling axis in regulating the malignant progression of cervical cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐367‐3p overexpression represses the proliferation and invasion of cervical cancer cells through downregulation of SPAG5‐mediated Wnt/β‐catenin signalling

Yang

Tian

Wang

et al. 2020

Clin Exp Pharma Physio

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“…For example, lncRNA XIST is significantly up-regulated in NSCLC tissues compared with adjacent normal tissues, XIST inhibits proliferation, migration, and invasion of NSCLC cells, and XIST induces G0/G1 phase arrest by sponging miR-367/141 [20]. In vivo experiments have shown that HOTAIR knockdown reduces tumor growth and invasion and enhances apoptosis and miR-613 expression [21].…”

Section: Discussionmentioning

confidence: 99%

“…Chen et al [23] showed the carcinogenic effect of FOXD2-AS1 in clinical specimens and in vitro cell experiments and revealed the potential pathway of FOXD2-AS1/miR-363-5p/S100A1. Li et al [20] found that lncRNA XIST promotes TGF-β-induced EMT, cell invasion, and metastasis by regulating the miR-367/miR-141-ZEB2 pathway in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

Gastric Adenocarcinoma Predictive Long Intergenic Non-Coding RNA Promotes Tumor Occurrence and Progression in Non-Small Cell Lung Cancer via Regulation of the miR-661/eEF2K Signaling Pathway

Gu¹,

Chen²,

Song³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long non-coding RNAs (lncRNAs) play vital roles in carcinogenesis as oncogenes or tumor suppressor genes. This study explored the biological function of lncRNA gastric adenocarcinoma predictive long intergenic non-coding RNA (GAPLINC) in human non-small cell lung cancer (NSCLC). Methods: GAPLINC expression in NSCLC specimens and cell lines was detected by qRT-PCR and Western blot. The effect of GAPLINC on cell proliferation was investigated using CCK8-assay, colony formation assay, and xenograft model. The effects of GAPLINC on apoptosis and cell cycle were determined using flow cytometry. The mechanism of GAPLINC involved in NSCLC was explored using Western blot, luciferase reporter assay, and RNA fluorescence in situ hybridization. Results: We found that GAPLINC expression was up-regulated in NSCLC tissues and cell lines. Overexpression of GAPLINC was associated with poor prognosis in patients with NSCLC. Silencing of GAPLINC significantly inhibited cell proliferation, promoted apoptosis, and induced cell cycle arrest in the G0/G1 phase. Results from xenograft transplantation showed that GAPLINC silencing inhibited the tumor growth in vivo. Interestingly, GAPLINC silencing decreased the expression of eukaryotic elongation factor-2 kinase (eEF2K) protein both in vivo and in vitro. Bioinformatic analysis and luciferase reporter confirmed that miR-661 targeted GAPLINC and eEF2K 3’-UTR and was negatively correlated with the expression of GAPLINC and eEF2K. Conclusion: Our findings indicate that GAPLINC promotes NSCLC tumorigenesis by regulating miR-661/eEF2K cascade and provide new insights for the pathogenesis underlying NSCLC and potential targets for therapeutic strategy.

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“…Fast‐growing number of studies have disclosed that dysregulations of lncRNAs are correlated with various diseases including cancers, neurodegeneration diseases, cardiovascular diseases, and inflammatory diseases, as well as lung cancer and pulmonary fibrosis . The lncRNA X inactivate‐specific transcript (XIST), which is located on the X chromosome, is enriched in multiple cancers and regulates tumorigenesis and development as a potential oncogene gene through competing RNA mechanisms . Of note, XIST is proved to regulate the inflammatory response in neuropathic pain and peripheral nerve injury .…”

Section: Introductionmentioning

confidence: 99%

Knockdown XIST alleviates LPS‐induced WI‐38 cell apoptosis and inflammation injury via targeting miR‐370‐3p/TLR4 in acute pneumonia

Zhang

Zhu

Gao

et al. 2019

Cell Biochemistry & Function

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Pneumonia is an inflammatory disease that occurs in the lungs associated with pathogens or other factors. It has been well established that long noncoding RNA X inactivate‐specific transcript (XIST) is involved in several cancers. The present study focused on the effect and detailed mechanism of XIST in lipopolysaccharide (LPS)‐induced injury in pneumonia. Here, XIST was silenced by transfection with XIST‐targeted siRNA, and then, mRNA expression, cell viability, apoptosis, and protein expression were, respectively, assessed by qRT‐PCR, CCK‐8, flow cytometry, and Western blotting. Luciferase reporter, RIP, and RNA pull‐down assays were used to detect the combination of miR‐370‐3p and XIST. Besides, the tested proinflammatory factors were analysed by qRT‐PCR and Western blot, and their productions were quantified by ELISA. The results showed that XIST expression was robustly increased in serum of patients with acute‐stage pneumonia and LPS‐induced WI‐38 human lung fibroblasts cells. Functional analyses demonstrated that knockdown of XIST remarkably alleviated LPS‐induced cell injury through increasing cell viability and inhibiting apoptosis and inflammatory cytokine levels. Mechanistically, XIST functioned as a competitive endogenous RNA (ceRNA) by effectively binding to miR‐370‐3p and then restoring TLR4 expression. More importantly, miR‐370‐3p inhibitor abolished the function of XIST knockdown on cell injury and JAK/STAT and NF‐κB pathways. Taken together, XIST may be involved in progression of cell inflammatory response, and XIST/miR‐370‐3p/TLR4 axis thus may shed light on the development of novel therapeutics to the treatment of acute stage of pneumonia. Significance of the study Our study demonstrated that XIST was highly expressed in patients with acute stage of pneumonia. Knockdown of XIST remarkably alleviated LPS‐induced cell injury through increasing cell viability and inhibiting apoptosis and inflammatory cytokine levels through regulating JAK/STAT and NF‐κB pathways.

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Long non-coding RNA XIST promotes TGF-β-induced epithelial-mesenchymal transition by regulating miR-367/141-ZEB2 axis in non-small-cell lung cancer

Cited by 155 publications

References 51 publications

MicroRNA‐367‐3p overexpression represses the proliferation and invasion of cervical cancer cells through downregulation of SPAG5‐mediated Wnt/β‐catenin signalling

MicroRNA‐367‐3p overexpression represses the proliferation and invasion of cervical cancer cells through downregulation of SPAG5‐mediated Wnt/β‐catenin signalling

Gastric Adenocarcinoma Predictive Long Intergenic Non-Coding RNA Promotes Tumor Occurrence and Progression in Non-Small Cell Lung Cancer via Regulation of the miR-661/eEF2K Signaling Pathway

Knockdown XIST alleviates LPS‐induced WI‐38 cell apoptosis and inflammation injury via targeting miR‐370‐3p/TLR4 in acute pneumonia

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