Hedgehog Suppresses Paclitaxel Sensitivity Through Regulating Akt-Mediated Phosphorylation of Bax in EGFR Wild Type Non-Small Cell Lung Cancer Cells.

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題名:	Hedgehog Suppresses Paclitaxel Sensitivity Through Regulating Akt-Mediated Phosphorylation of Bax in EGFR Wild Type Non-Small Cell Lung Cancer Cells.
作者:	蘇柏全 Yun Chieh Tu, Wei Chen Yeh, Hsin Hsien Yu, Yu Cheng Lee, Bor Chyuan Su
貢獻者:	醫學系解剖學暨細胞生物學科
關鍵詞:	Keywords: EGFR;GDC-0449;Hedgehog;non-small cell lung cancer;paclitaxel
日期:	2022-02
上傳時間:	2025-03-30 15:38:56 (UTC+8)
摘要:	Abstract Non-small cell lung cancer (NSCLC) is one of the most common and deadly cancers worldwide. Among NSCLC patients, almost half have wild-type epidermal growth factor receptor (EGFR WT). The primary therapeutic option for these EGFR WT NSCLC patients is chemotherapy, while NSCLC patients with EGFR mutations have more diverse therapeutic options, including EGFR tyrosine kinase inhibitors. Moreover, NSCLC patients with EGFR WT have worse chemotherapy response than EGFR mutant NSCLC patients. Thus, an urgent need exists for novel therapeutic strategies to improve chemotherapy response in EGFR WT NSCLC patients. Hedgehog signaling is known to be highly active in NSCLC; however, its potential role in chemoresistance is not fully understood. In the present study, we found that paclitaxel (PTX) treatment induces hedgehog signaling in EGFR WT NSCLC cells, and inhibition of hedgehog signaling with GDC-0449 (Vismodegib) increases sensitivity to PTX-stimulated apoptosis. Furthermore, GDC-0449 potentiates PTX-induced reactive oxygen species and mitochondrial dysfunction. In contrast, a hedgehog agonist, Hh-Ag1.5, attenuates PTX-induced apoptosis. Mechanistic experiments revealed that hedgehog induces phosphorylation of Akt at Ser473. Akt then phosphorylates Bax at Ser184, which can switch its activity from pro-apoptosis to anti-apoptosis. Taken together, our findings suggest that inhibition of hedgehog signaling might be a promising therapeutic strategy to improve PTX response in EGFR WT NSCLC.
關聯:	Front Pharmacol. 2022 Feb 18:13:815308
描述:	【111-2 升等】臺北醫學大學教師升等專門著作職別：專任教師送審等級：副教授著作送審
資料類型:	article
顯示於類別:	[教師升等送審著作] 111

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