B-Cell Translocation Gene 2 Upregulation Is Associated with Favorable Prognosis in Lung Adenocarcinoma and Prolonged Patient Survival

Author:

Liang Junting1,Cheng Linna2,Gao Haiyan3,Fu Wanying4,Zhang Xiulei5ORCID,Zhang Jianhua6,Li Jinming7ORCID,Chen Chuanliang1ORCID

Affiliation:

1. Clinical Bioinformatics Experimental Center, Henan Provincial People’s Hospital, People’s Hospital of Zhengzhou University, Zhengzhou, 450003 Henan, China

2. Institute of Hematology, Henan Key Laboratory of Stem Cell Differentiation and Modification, Henan Provincial People’s Hospital, Zhengzhou University People’s Hospital, Henan University People’s Hospital, Zhengzhou, 450003 Henan, China

3. Henan Key Laboratory of Neurological Imaging, Henan Provincial People’s Hospital, People’s Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450003 Henan, China

4. School of Basic Medicine, Xinxiang Medical University, Xinxiang, 453003 Henan, China

5. Department of Microbiome Laboratory, Henan Provincial People’s Hospital, People’s Hospital of Zhengzhou University, Zhengzhou, 450003 Henan, China

6. Medical Engineering Technology and Data Mining Institute of Zhengzhou University, Zhengzhou, 450000 Henan, China

7. The Translational Research Institute, Henan Provincial People’s Hospital, School of Medicine, Zhengzhou University, Zhengzhou, 450003 Henan, China

Abstract

The tumor suppressor protein B-cell translocation gene 2 (BTG2) is downexpressed in lung adenocarcinoma (LUAD); however, its role in LUAD survival remains unknown. This investigation is aimed at exploring the activity of BTG2 in LUAD. We analyzed BTG2 expression in LUAD datasets of the TCGA database and examined that BTG2 was markedly downregulated in comparison with adjacent normal tissues. The prognostic analysis suggested that higher expression of BTG2 protein correlates with prolonged survival in patients. Vectors expressing BTG2 were stably transduced into lung adenocarcinoma A549 cells. The overexpression of BTG2 in A549 cells causes cellular G1 phase arrest but did not affect cell proliferation, accompanied by increased activation of NF-κB. Our data indicate that BTG2 overexpression may trigger an autoregulatory prosurvival NF-κB pathway, which is resistant to environmental intervention owing to an increased level of BTG2.

Funder

Key Project of Henan Province Medical Science and Technology Project

Publisher

Hindawi Limited

Subject

Oncology

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