B7-H3 promotes metastasis, proliferation, and epithelial-mesenchymal transition in lung adenocarcinoma
Authors Yu TT, Zhang T, Lu X, Wang RZ
Received 31 March 2018
Accepted for publication 20 July 2018
Published 10 August 2018 Volume 2018:11 Pages 4693—4700
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 4
Editor who approved publication: Dr Samir Farghaly
Ting-Ting Yu,1,* Tao Zhang,2,* Xi Lu,3 Ruo-Zheng Wang3
1Department of Thoracic Oncology, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi 830011, People’s Republic of China; 2Department of Oncology, The First Hospital of Lanzhou University, Lanzhou 730000, People’s Republic of China; 3Radiation Therapy Center, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi 830011, People’s Republic of China
*These authors contributed equally to this work
Background: Lung adenocarcinoma is the most common pathological type of lung cancer. However, the mechanisms underlying its development are still poorly understood. B7-H3 was discovered as a new member of the B7 costimulatory family.
Methods: We detected the expression status of B7-H3 protein in lung adenocarcinoma tissues, and evaluated the relationship of B7-H3 expression and patients’ prognosis. Then, we silenced its expression in A549 cells by transient siRNA transfection to ascertain the function of B7-H3 in lung adenocarcinoma cells. Western blotting was used to detect the expression of epithelial–mesenchymal transition (EMT) related proteins.
Results: We found that B7-H3 overexpressed in lung adenocarcinoma. It is correlated with lymph node metastasis, distant metastasis, and disease stage. The Cox regression analysis showed that B7-H3 might serve as an independent prognostic marker of lung adenocarcinoma. We also found that B7-H3 promoted proliferation, invasion and migration of A549 cells in vitro. B7-H3 also could promote EMT progression by regulating EMT-related molecules.
Conclusion: B7-H3 is a potential target for the treatment of lung adenocarcinoma.
Keywords: lung adenocarcinoma, B7-H3, epithelial–mesenchymal transition, metastasis, proliferation
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