Heptadecanoic acid inhibits cell proliferation in PC‑9 non‑small‑cell lung cancer cells with acquired gefitinib resistance | Zendy

Changzhi Xu | Zendy; Pengfei Wu | Zendy; Jiajia Gao | Zendy; Lanlan Zhang | Zendy; Tengfei Ma | Zendy; Bingbing Ma | Zendy; Shuai Yang | Zendy; Guojian Shao | Zendy; Yang Yu | Zendy; Xunduan Huang | Zendy; Xingyuan Yang | Zendy; Buchang Zhang | Zendy

Open Access

Heptadecanoic acid inhibits cell proliferation in PC‑9 non‑small‑cell lung cancer cells with acquired gefitinib resistance

Author(s) -

Changzhi Xu,

Pengfei Wu,

Jiajia Gao,

Lanlan Zhang,

Tengfei Ma,

Bingbing Ma,

Shuai Yang,

Guojian Shao,

Yang Yu,

Xunduan Huang,

Xingyuan Yang,

Buchang Zhang

Publication year - 2019

Publication title -

oncology reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.094

H-Index - 96

eISSN - 1791-2431

pISSN - 1021-335X

DOI - 10.3892/or.2019.7130

Subject(s) - gefitinib , apoptosis , cell growth , cancer research , protein kinase b , cell cycle , cell , oncogene , lung cancer , pi3k/akt/mtor pathway , signal transduction , cytotoxicity , biology , chemistry , cancer , medicine , microbiology and biotechnology , in vitro , epidermal growth factor receptor , biochemistry

Non‑small cell lung carcinomas (NSCLC) are common and are the leading cause of cancer‑associated mortality worldwide. Heptadecanoic acid (C17:0) is an odd‑chain saturated fatty acid. The effect of C17:0 on lung cancer has remained elusive. The present study examined the role of C17:0 in the PC‑9 NSCLC cell line and PC‑9 cells with acquired‑gefitinib resistance (PC‑9/GR) in vitro. Cell proliferation, migration, apoptosis, fatty acid composition and the activation of relevant signaling pathways were assessed. The results indicated that C17:0 significantly inhibited cell proliferation, and migration, while promoting apoptosis in PC‑9 and PC‑9/GR cells. Furthermore, C17:0 enhanced the cytotoxicity of gefitinib to PC‑9 and PC‑9/GR cells. Mechanistical analysis indicated that the activation of the phosphoinositide 3‑kinase/Akt signaling pathway was suppressed in C17:0‑treated PC‑9 and PC‑9/GR cells. Furthermore, the addition of C17:0 led to accumulation of 10‑cis‑heptadecenoic acid in NSCLC cells. Collectively, the present study demonstrated that C17:0 is an effective agent against NSCLC cells in vitro and the results may imply that the intake of C17:1 or C17:0‑rich food may be beneficial during the treatment of NSCLC.

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