High glucose contributes to the proliferation and migration of non-small-cell lung cancer cells via GAS5-TRIB3 axis

Ding, Chengzhi; Guo, Xufeng; Wang, Guolei; Wang, Hong-Tao; Xu, Guanghui; Liu, Yuan-Yuan; Wu, Zhen-Jiang; Chen, Yuhang; Wang, Jiao; Wang, Wenguang

doi:10.1042/bsr20171014

Cited by 31 publications

(15 citation statements)

References 27 publications

(27 reference statements)

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“…48 GAS5 inhibited the high glucose (HG)-induced proliferation, anti-apoptosis, and migration of PC-9 and H1299 NSCLC cells through degradation of tribbles pseudokinase 3 (TRIB3) protein by ubiquitination, indicating that GAS5/TRIB3 might be novel targets for the prevention and treatment of diabetic NSCLC. 121 In addition, exogenously expressed GAS5 repressed cell proliferation and invasion and enhanced the radiosensitivity of NSCLC cells in vitro and in vivo by suppressing miR-135b expression, which deepens our understanding of the mechanism of miRNA-lncRNA interaction and providing a potential therapeutic for patients with NSCLC. 43 Moreover, GAS5 inhibited the proliferation and colony formation capability of NSCLC cells and induced the sensitivity of DDP in NSCLC via GAS5/miR-21/PTEN regulatory pathway.…”

Section: Molecular Mechanismsmentioning

confidence: 98%

Novel Tumor Suppressor lncRNA Growth Arrest-Specific 5 (GAS5) In Human Cancer

Yu¹,

Hann²

2019

OTT

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Long noncoding RNAs (lncRNAs) play crucial regulatory roles in fundamental biological processes, and deregulations of lncRNAs have been linked to numerous human diseases, especially cancers. Of particular interest in this regard is lncRNA GAS5, which is mainly identified as a tumor suppressor in several cancers. GAS5 was significantly low expressed in multiple cancers and was associated with clinic-pathological characteristics and patient survival, indicating a novel potential diagnostic and prognostic biomarker, and a therapeutic target for cancer. Functionally, GAS5 is involved in cell proliferation, metastasis, invasion, apoptosis, epithelial-mesenchymal transition (EMT), and drug resistance, among others, via multiple molecular mechanisms, such as binding to DNA sequences, forming RNA-DNA triplex complex, triggering or suppressing the expression of genes, binding proteins to form chromatin-modifying complex, which activates or represses gene expression, and acting as miRNA sponge to suppress miRNA expression, leading to regulation of miRNA target genes. This review provides an overview of the current state of knowledge and role of GAS5 in clinical relevance, biological functions and molecular mechanisms underlying the dysregulation of expression and function of GAS5 in cancer. Finally, the potential prospective role as diagnostic and prognostic biomarker and therapeutic target in cancer is discussed.

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Section: Molecular Mechanismsmentioning

confidence: 98%

Novel Tumor Suppressor lncRNA Growth Arrest-Specific 5 (GAS5) In Human Cancer

Yu¹,

Hann²

2019

OTT

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“…The cells were cultured in DMEM containing high glucose (HG; 25 mM) or normal glucose (NG; 5 mM) with 10% foetal bovine serum, penicillin (100 U/mL) and streptomycin (100 U/mL) at 37°C in a 5% CO 2 humidified incubator (Thermo Fisher). HG treatment was used to induce the model of DM combined with A549 for 24 h. 22…”

Section: Cell Culturementioning

confidence: 99%

Mitofusin1 Is a Major Mediator in Glucose-Induced Epithelial-to-Mesenchymal Transition in Lung Adenocarcinoma Cells

Liu¹,

Feng²,

Wei³

et al. 2020

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Background: Epithelial-to-mesenchymal transition (EMT) has been considered a latent mediator of diverse biological processes in cancer. However, the mechanisms involved in high glucose-associated EMT in lung adenocarcinoma (LAD) have not been fully clarified. In this study, we aimed to investigate whether mitofusin1 (MFN1) is involved in the EMT of LAD cells induced by glucose and to identify the molecular mechanism involved in this process. Materials and Methods: The expression of specific proteins was analysed by Western blotting, immunohistochemistry, co-immunoprecipitation and immunofluorescence analysis. The proliferation, migration and invasion of cells were assessed by Cell Counting Kit-8, bromodeoxyuridine incorporation, wound-healing and transwell assays. Lung tissues of adjacent normal regions and lung tissues from patients with LAD and LAD combined with diabetes mellitus were collected to determine the expression and significance of MFN1. Results: Here, we showed that the expression of MFN1 was increased in LAD tissues compared with adjacent normal tissues and expression was even higher in lung tissues from patients with LAD combined with diabetes. In the lung cancer cell line A549, increased cell proliferation, invasion and EMT induced by high glucose were inhibited by MFN1 silencing. Mechanistic studies demonstrated that inhibiting autophagy reversed the abnormal EMT triggered by high glucose conditions. In addition, our data provide novel evidence demonstrating that PTEN-induced kinase (Pink) is a potential regulator involved in MFN1mediated cell autophagy, which eventually leads to high glucose-induced proliferation, invasion and EMT of A549 cells. Conclusion: Taken together, our data show that MFN1 interacts with Pink to induce the autophagic process and that the abnormal occurrence of autophagy ultimately contributes to glucose-induced pathological EMT in LAD.

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“…In the study of Zhang X et al, pseudokinase can activate the b-catenin signal pathway, which in turn promotes the proliferation and migration of NSCLC cells (Zhang et al, 2019). In addition, blocking the activity of TRIB3 may be one of the mechanisms for the treatment of lung cancer (Ding et al, 2018). Wang X et al have found that PAK4 is significantly associated with poor prognosis of NSCLC (Wang et al, 2016b), and LIMK1 phosphorylation mediated by it regulates the migration and invasion of NSCLC.…”

Section: The Biological Significance Of the Selected Genes In Lung Camentioning

confidence: 99%

The Functional Effects of Key Driver KRAS Mutations on Gene Expression in Lung Cancer

Zhang

et al. 2020

Front. Genet.

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Lung cancer is a common malignant cancer. Kirsten rat sarcoma oncogene (KRAS) mutations have been considered as a key driver for lung cancers. KRAS p.G12C mutations were most predominant in NSCLC which was comprised about 11-16% of lung adenocarcinomas (p.G12C accounts for 45-50% of mutant KRAS). But it is still not clear how the KRAS mutation triggers lung cancers. To study the molecular mechanisms of KRAS mutation in lung cancer. We analyzed the gene expression profiles of 156 KRAS mutation samples and other negative samples with two stage feature selection approach: (1) minimal Redundancy Maximal Relevance (mRMR) and (2) Incremental Feature Selection (IFS). At last, 41 predictive genes for KRAS mutation were identified and a KRAS mutation predictor was constructed. Its leave one out cross validation MCC was 0.879. Our results were helpful for understanding the roles of KRAS mutation in lung cancer.

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High glucose contributes to the proliferation and migration of non-small-cell lung cancer cells via GAS5-TRIB3 axis

Cited by 31 publications

References 27 publications

<p>Novel Tumor Suppressor lncRNA Growth Arrest-Specific 5 (GAS5) In Human Cancer</p>

<p>Novel Tumor Suppressor lncRNA Growth Arrest-Specific 5 (GAS5) In Human Cancer</p>

<p>Mitofusin1 Is a Major Mediator in Glucose-Induced Epithelial-to-Mesenchymal Transition in Lung Adenocarcinoma Cells</p>

The Functional Effects of Key Driver KRAS Mutations on Gene Expression in Lung Cancer

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