Dataset Information

Loss of CDKN2A at chromosome 9 has a poor clinical prognosis and promotes lung cancer progression.

ABSTRACT:

Objective

This study aimed to identify critical genes involved in the tumor biology of lung cancer via datamining of The Cancer Genome Atlas (TCGA) with special focus on gene copy number variation.

Methods

Genomic deletion and amplification were analyzed with cBioportal online tools. Relative expression of Cyclin Dependent Kinase Inhibitor 2A (CDKN2A) was analyzed by both real-time polymerase chain reaction (PCR) and Western blot. The abundance of methylthioadenosine phosphorylase (MTAP) and epithelial-mesenchymal transition markers were analyzed by real-time PCR. Cell proliferation was determined by cell counting kit-8 method and cell viability was measured with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The cell migration and invasion were measured with transwell chamber assay, and migrative capacity was further evaluated by wound healing assay.

Results

We found the frequent loss of CDKN2A was associated with its downregulation in lung cancer, and siRNA-mediated CDNKN2A knockdown significantly stimulated cell proliferation, invasion, and migration. Mechanistically, we unraveled that MTAP, which was positively correlated with CDKN2A, predominantly mediated the antitumoral function of CDKN2A in lung cancer.

Conclusion

Our study consolidated the involvement of CDKN2A-MTAP signaling in the context of lung cancer.

SUBMITTER: Liu W

PROVIDER: S-EPMC7767555 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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Publications

Loss of CDKN2A at chromosome 9 has a poor clinical prognosis and promotes lung cancer progression.

Liu Wei W Zhuang Congwen C Huang Tengfei T Yang Shengsheng S Zhang Meiqing M Lin Baoquan B Jiang Yi Y

Molecular genetics & genomic medicine 20201106 12

<h4>Objective</h4>This study aimed to identify critical genes involved in the tumor biology of lung cancer via datamining of The Cancer Genome Atlas (TCGA) with special focus on gene copy number variation.<h4>Methods</h4>Genomic deletion and amplification were analyzed with cBioportal online tools. Relative expression of Cyclin Dependent Kinase Inhibitor 2A (CDKN2A) was analyzed by both real-time polymerase chain reaction (PCR) and Western blot. The abundance of methylthioadenosine phosphorylase ...[more]

PMID: 33155773

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Project description:Background: MEOX1 is a homeobox transcriptional factor, and plays essential roles in regulating somite development. Our previous study indicated that MEOX1 is a critical molecular target in mesenchymal-like cancer cells in PTEN-deficient Trastuzumab resistant breast cancer. Despite the potential implication of MEOX1 for the cancer progression, no previous studies examined its level and clinical significance in lung cancer tissues. In this study, we aimed to detect the MEOX1 expression and correlate its level with clinical outcome in non-small-cell lung cancer patients (NSCLC). Methods: MEOX1 gene expression in lung cancer was examined by using the Oncomine database. MEOX1 protein levels were evaluated by IHC using the corresponding primary antibody on two different commercial lung cancer tissue arrays. siRNA knockdown was used to elucidate the function of MEOX1. Results: Analysis of the Oncomine datasets identified that an elevation of MEOX1 in gene amplification in lung cancer tissues in comparison to normal lung tissues. Immunohistochemistical analysis demonstrated that MEOX1 was localized predominantly in the nucleus, and positive rate was 67.3% (111/165) in NSCLC samples. Statistical analysis revealed high levels of MEOX1 significantly correlated with Lymph Node Metastasis and Stage. Kaplan-Meier survival analysis showed that high levels of MEOX1 were significantly associated with unfavorable survival in NSCLC patients, and MEOX1 nucleus staining had worse survival, than did patients with overall expression in lung squamous cell carcinoma patients. Multivariate Cox's regression analysis found that MEOX1 was an independent poor prognostic predictor for patients with NSCLC. Silencing of MEOX1 by specific SiRNA significantly inhibited H460 and H1299 cell proliferation and sphere formation in serum-free medium. Conclusions: Our results firstly indentified that high levels of MEOX1 especially nuclear staining was an independent prognostic factor for NSCLC, and it served a essential roles in the regulation of cell proliferation and colony formation in vitro. It may represent a potential target for the NSCLC treatment.

Dataset Information

Loss of CDKN2A at chromosome 9 has a poor clinical prognosis and promotes lung cancer progression.

Objective

Methods

Results

Conclusion

Publications

Loss of CDKN2A at chromosome 9 has a poor clinical prognosis and promotes lung cancer progression.

Similar Datasets

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