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

Abstract

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.