9 5 7 4 9
论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
- 3.3 Breast Cancer (Dove Med Press)
- 3.4 Clin Epidemiol
- 2.5 Cancer Manag Res
- 2.9 Infect Drug Resist
- 3.5 Clin Interv Aging
- 4.7 Drug Des Dev Ther
- 2.7 Int J Chronic Obstr
- 6.6 Int J Nanomed
- 2.5 Int J Women's Health
- 2.5 Neuropsych Dis Treat
- 2.7 OncoTargets Ther
- 2.0 Patient Prefer Adher
- 2.3 Ther Clin Risk Manag
- 2.5 J Pain Res
- 2.8 Diabet Metab Synd Ob
- 2.8 Psychol Res Behav Ma
- 3.0 Nat Sci Sleep
- 1.8 Pharmgenomics Pers Med
- 2.7 Risk Manag Healthc Policy
- 4.2 J Inflamm Res
- 2.1 Int J Gen Med
- 4.2 J Hepatocell Carcinoma
- 3.7 J Asthma Allergy
- 1.9 Clin Cosmet Investig Dermatol
- 2.7 J Multidiscip Healthc
已发表论文
FAM98A 通过 P38-ATF2 信号传导途径促进非小细胞肺癌细胞的增殖
Authors Zheng R, Liu Q, Wang T, Wang L, Zhang Y
Received 21 January 2018
Accepted for publication 13 April 2018
Published 27 July 2018 Volume 2018:10 Pages 2269—2278
DOI https://doi.org/10.2147/CMAR.S163323
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 4
Editor who approved publication: Professor Nakshatri
Background: FAM98A, a novel
protein, is expressed in ovarian and colorectal cancer tissues. However, the
association between FAM98A expression and the clinicopathological
characteristics of non-small cell lung cancer (NSCLC) remains undetermined.
Materials and methods: The FAM98A expression pattern was determined in NSCLC samples and corresponding adjacent normal lung tissues using immunohistochemical staining and Western blotting. The association of FAM98A expression with clinicopathological characteristics was measured in 131 NSCLC samples. Finally, the overexpression and inhibition of FAM98A was performed in the A549 and SPC-A1 cell lines to explore its role in the development of lung cancer.
Results: Western blot analysis of 20 paired NSCLC samples showed that expression of FAM98A was higher in lung cancer tissues than in the corresponding adjacent normal lung tissues (p <0.05). Immunohistochemical staining of 128 NSCLC specimens showed that expression of FAM98A was significantly higher in lung cancer samples than in adjacent normal lung tissues (118/128 vs 10/128; p <0.001). Positive expression of FAM98A was significantly related to tumor TNM stage (p <0.05) and lymph node metastasis (p <0.001). Additionally, overexpression of FAM98A induced an increase in the expression of phosphorylated P38, phosphorylated ATF2, and cyclin D1, which promoted proliferation of lung cancer cells. Correspondingly, the effects of FAM98A overexpression were reversed by administration of a specific inhibitor of phosphorylated P38.
Conclusion: FAM98A was overexpressed in the cytoplasm of NSCLC samples and correlated with advanced TNM staging and lymph node metastasis. Thus, FAM98A increases the expression of cyclin D1 by activating the P38-ATF2 signaling pathway and subsequently enhancing tumor cell proliferation; these results are promising and need further validation.
Keywords: ATF2, TNM stage, lymph node metastasis
Materials and methods: The FAM98A expression pattern was determined in NSCLC samples and corresponding adjacent normal lung tissues using immunohistochemical staining and Western blotting. The association of FAM98A expression with clinicopathological characteristics was measured in 131 NSCLC samples. Finally, the overexpression and inhibition of FAM98A was performed in the A549 and SPC-A1 cell lines to explore its role in the development of lung cancer.
Results: Western blot analysis of 20 paired NSCLC samples showed that expression of FAM98A was higher in lung cancer tissues than in the corresponding adjacent normal lung tissues (p <0.05). Immunohistochemical staining of 128 NSCLC specimens showed that expression of FAM98A was significantly higher in lung cancer samples than in adjacent normal lung tissues (118/128 vs 10/128; p <0.001). Positive expression of FAM98A was significantly related to tumor TNM stage (p <0.05) and lymph node metastasis (p <0.001). Additionally, overexpression of FAM98A induced an increase in the expression of phosphorylated P38, phosphorylated ATF2, and cyclin D1, which promoted proliferation of lung cancer cells. Correspondingly, the effects of FAM98A overexpression were reversed by administration of a specific inhibitor of phosphorylated P38.
Conclusion: FAM98A was overexpressed in the cytoplasm of NSCLC samples and correlated with advanced TNM staging and lymph node metastasis. Thus, FAM98A increases the expression of cyclin D1 by activating the P38-ATF2 signaling pathway and subsequently enhancing tumor cell proliferation; these results are promising and need further validation.
Keywords: ATF2, TNM stage, lymph node metastasis
