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首页> 外文期刊>Journal of 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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Knockdown of Tubulin Polymerization Promoting Protein Family Member 3 Suppresses Proliferation and Induces Apoptosis in Non-Small-Cell Lung Cancer

机译:肾小管聚合促进蛋白家族成员3的基因抑制抑制增殖,并诱导非小细胞肺癌细胞凋亡。

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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.
机译:我们以前的研究表明,微管蛋白聚合促进蛋白家族成员3(TPPP3)的耗竭抑制增殖并诱导HeLa细胞凋亡。但是,TPPP3在癌症中的表达和作用仍然未知。在这项研究中,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中的表达。 TPPP3表达在NSCLC组织中显着上调,而高TPPP3表达与肿瘤大小,淋巴结转移,临床分期和不良生存呈正相关。此外,shRNA敲低TPPP3可以显着抑制细胞增殖,并在体外诱导细胞凋亡和细胞周期停滞。此外,在H1299细胞的异种移植物中,TPPP3的耗竭抑制了体内肺癌的生长。该作用伴随着Ki67表达的抑制。我们的数据表明TPPP3可能是NSCLC中的癌基因。 TPPP3值得考虑作为具有抗肿瘤潜力的治疗候选药物。

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