Farnesiferol c induces apoptosis via regulation of L11 and c-Myc with combinational potential with anticancer drugs in non-small-cell lung cancers

• DOI: 10.1038/srep26844
• Publication Date: 2016-05-27T09:22:04Z
• Authors: Ji Hoon Jung; Moon Joon Kim; Hyemin Lee; Jihyun Lee; Jaekwang Kim; Hyun Joo Lee; Eun Ah Shin; Yoon Hyeon Kim; Bonglee Kim; Bum Sang Shim; Sung-Hoon Kim
• Keywords: Nucleolin; Survivin; Puromycin

Abstract Though Farnesiferol c (FC) has been reported to have anti-angiogenic and antitumor activity, the underlying mechanism of FC still remains unclear. Thus, in present study, we investigated apoptotic human H1299 H596 non-small lung cancer cells (NSCLCs). significantly showed cytotoxicity, increased sub-G1 accumulation, attenuated expression Bcl-2, Bcl-xL, Survivin procaspase 3 cells. Furthermore, effectively suppressed mRNA G1 arrest related genes such as Cyclin D1, E2F1 transcription factor CDC25A by RT-PCR. Interestingly, inhibited c-Myc, ribosomal protein L11 (L11) nucleolin (NCL) Of note, silencing siRNA transfection enhanced c-Myc through a negative feedback mechanism, while knockdown downregulated Additionally, combined treatment puromycin/doxorubicin promoted activation caspase 9/3, D1 CDK4 compared single treatment. Taken together, our findings suggest that induces apoptosis via regulation also enhances effect puromycin or doxorubicin NSCLCs.