1. Knockdown of Tubulin Polymerization Promoting Protein Family Member 3 Suppresses Proliferation and Induces Apoptosis in Non-Small-Cell Lung Cancer
- Author
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Min He, Wenbai Zhou, Kuanping Ye, Bin Lu, Nan Wu, Yali Xu, Naijia Liu, Renming Hu, Junfeng Li, and Yintao Li
- Subjects
0301 basic medicine ,Gene knockdown ,Cell cycle checkpoint ,biology ,Oncogene ,Cell growth ,NSCLC ,medicine.disease ,biology.organism_classification ,cell apoptosis ,Cell biology ,HeLa ,Small hairpin RNA ,03 medical and health sciences ,cell proliferation ,030104 developmental biology ,0302 clinical medicine ,Oncology ,Apoptosis ,030220 oncology & carcinogenesis ,medicine ,Lung cancer ,TPPP3 ,Research Paper - Abstract
Our previous studies demonstrated that depletion of tubulin polymerization promoting protein family member 3 (TPPP3) inhibits proliferation and induces apoptosis of HeLa cells. However, the expression and roles of TPPP3 in cancers remain largely unknown. In this study, we investigated the expression of TPPP3 in clinicopathological correlations in non-small-cell lung cancer (NSCLC) samples by immunohistochemistry. TPPP3 expression was significantly upregulated in NSCLC tissues, and high TPPP3 expression was positively associated with tumor size, lymph node metastasis, clinical stage, and poor survival. Furthermore, knockdown of TPPP3 by shRNA significantly inhibited cell proliferation and induced cell apoptosis and cell cycle arrest in vitro. In addition, depletion of TPPP3 inhibited lung cancer growth in vivo in the xenografts of H1299 cells; this effect was accompanied by the suppression of Ki67 expression. Our data suggested that TPPP3 might act as an oncogene in NSCLC. TPPP3 warrants consideration as a therapeutic candidate with anti-tumor potential.
- Published
- 2016