TetR family transcriptional regulators (TFRs) are generally found to regulate diverse cellular processes in bacteria, especially antibiotic biosynthesis in Streptomyces species. However, knowledge of their function in lincomycin biosynthesis in S. lincolnensis remains unknown. The present study provides a new insight into the regulation of lincomycin biosynthesis through a TFR, SLCG_2919, that directly modulates lincomycin production and resistance. Intriguingly, SLCG_2919 and its adjoining gene, SLCG_2920 , which encodes an ATP/GTP binding protein, were extensively distributed in diverse Streptomyces species. In addition, we revealed a new TFR binding motif, in which SLCG_2919 binds to the promoter region of SLCG_2920 , dependent on the intervening AT-rich sequence rather than on the flanking inverted repeats found in the binding sites of other TFRs. These insights into transcriptional regulation of lincomycin biosynthesis by SLCG_2919 will be valuable in paving the way for genetic engineering of regulatory elements in Streptomyces species to improve antibiotic production.

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.