期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 20, 期 23, 页码 -出版社
MDPI
DOI: 10.3390/ijms20235914
关键词
emetine; cisplatin resistance; lung cancer; Wnt/beta-catenin
资金
- Ministry of Science and Technology, Taiwan, Republic of China [MOST 105-2314-B-016-049, MOST 107-2314-B-016-012, MOST 105-2320-B-016-017-MY3]
- Ministry of National Defense, Taiwan, Republic of China [MAB-107-026, MAB-107-027, MAB-107-028, MAB-108-012, MAB-108-013, MAB-108-014, MAB-108-015]
- Tri-Service General Hospital, Taiwan, Republic of China [TSGH-C107-014, TSGH-C107-049, TSGH-C108-072]
y Cisplatin is still the primary therapeutic choice for advanced lung cancers without driver mutations. The occurrence of cisplatin resistance is a major clinical problem in lung cancer treatment. The natural extracted agent emetine reportedly has anticancer effects. This study aimed to explore the possible role of emetine in cisplatin resistance. We used cell viability, Western blot, and Wnt reporter assays to show that emetine suppresses proliferation, beta-catenin expression, and Wnt/beta-catenin signaling in non-small cell lung cancer (NSCLC). The synergism of emetine and cisplatin was assessed by constructing isobolograms and calculating combination index (CI) values using the Chou-Talalay method. Emetine effectively synergized with cisplatin to suppress the proliferation of cancer cells. Furthermore, nuclear beta-catenin and cancer stem cell-related markers were upregulated in the cisplatin-resistant subpopulation of CL1-0 cells. Emetine enhanced the anticancer efficacy of cisplatin and synergized with cisplatin in the cisplatin-resistant subpopulation of CL1-0 cells. Taken together, these data suggest that emetine could suppress the growth of NSCLC cells through the Wnt/beta-catenin pathway and contribute to a synergistic effect in combination with cisplatin.
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