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J Cancer. 2016 Jun 18;7(10):1189-96. doi: 10.7150/jca.14790. eCollection 2016.

Knockdown of Tubulin Polymerization Promoting Protein Family Member 3 Suppresses Proliferation and Induces Apoptosis in Non-Small-Cell Lung Cancer.

Li Y1, Xu Y2, Ye K3, Wu N4, Li J5, Liu N3, He M3, Lu B3, Zhou W3, Hu R3.

Author information

1
1. Department of Endocrinology and Metabolism, Institute of Endocrinology and Diabetology, Huashan Hospital, Fudan University, Shanghai, P.R. China; 2. Department of Medical Oncology, Shandong Cancer Hospital and Institute, Jinan, Shandong, P.R. China.
2
3. Department of Pathology, Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, P.R. China.
3
1. Department of Endocrinology and Metabolism, Institute of Endocrinology and Diabetology, Huashan Hospital, Fudan University, Shanghai, P.R. China.
4
4. Department of Geriatrics, Zhongshan Hospital, Fudan University, Shanghai, P.R. China.
5
5. Department of Endocrinology, Renmin Hospital of Wuhan University, Wuhan, Hubei, P.R. China.

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.

KEYWORDS:

NSCLC; TPPP3; cell apoptosis.; cell proliferation

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