Knockdown of Tubulin Polymerization Promoting Protein Family Member 3 Suppresses Proliferation and Induces Apoptosis in Non-Small-Cell Lung Cancer.
Knockdown of Tubulin Polymerization Promoting Protein Family Member 3 Suppresses Proliferation and Induces Apoptosis in Non-Small-Cell Lung Cancer.
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微管蛋白聚合促进蛋白家族成员 3 的敲低可抑制非小细胞肺癌的增殖并诱导细胞凋亡
DOI：
10.7150/jca.14790
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发表时间：
2016
影响因子：
3.9
通讯作者：
Hu R
中科院分区：
文献类型：
--
作者：
Li Y;Xu Y;Ye K;Wu N;Li J;Liu N;He M;Lu B;Zhou W;Hu R
我们之前的研究表明，微管蛋白聚合促进蛋白家族成员3 （TPPP3）的缺失可以抑制HeLa细胞的增殖并诱导细胞凋亡。然而，TPPP3在癌症中的表达和作用在很大程度上仍然未知。在本研究中，我们通过免疫组织化学研究了TPPP3在非小细胞肺癌（NSCLC）样本中临床病理相关性的表达。TPPP3在NSCLC组织中表达显著上调，且TPPP3高表达与肿瘤大小、淋巴结转移、临床分期、生存不良呈正相关。此外，shRNA敲低TPPP3可显著抑制细胞增殖，诱导细胞凋亡和细胞周期阻滞。此外，TPPP3的缺失抑制了H1299细胞异种移植体内肺癌的生长；这种作用伴随着Ki67表达的抑制。我们的数据表明TPPP3可能在NSCLC中起致癌基因的作用。TPPP3作为一种具有抗肿瘤潜力的候选治疗药物值得考虑。
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.