STK33-Dependent Transcriptional Regulation of SFTA3 Induces Cisplatin- Resistance in Lung Adenocarcinoma

(E-pub Ahead of Print)

Author(s): Kuilong Zhou, Runzhi Dong, Zhiheng Wang, Zhian Tang, Xuezhen Gao, Yaqing Du, Xiaoli Zhang, Xiangying Li, Qingfan Xie*.

Journal Name: Anti-Cancer Agents in Medicinal Chemistry
(Formerly Current Medicinal Chemistry - Anti-Cancer Agents)

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Drug-resistance has become a major obstacle for Cisplatin usage in non-small cell lung cancer. In this study, we identified a poorly-studied kinase Serine/Threonine Kinase 33 (STK33) as the most up-regulated kinase encoding gene in Cisplatin resistant lung adenocarcinoma. Additionally, STK33-dependent Cisplatin-resistance promotes tumor growth of lung adenocarcinoma both in vitro and in vivo. Clinically, STK33 expression was enriched in lung adenocarcinoma and was correlated to poor prognosis of lung cancer patients. Mechanically, STK33 promoted cell growth and Cisplatin-resistance of lung adenocarcinoma via transcriptional regulation of surfactant associated 3 (SFTA3), indicating that STK33-SFTA3 signaling axis could be a potential therapeutic target for Cisplatin-resistant lung adenocarcinoma.

Keywords: STK33, SFTA3, cisplatin-resistant, lung adenocarcinoma

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(E-pub Ahead of Print)
DOI: 10.2174/1871520619666190507100912
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