Ribosomal proteinL5mediated inhibition ofc-Mycis critically involved in sanggenon G induced apoptosis in non-small lung cancer cells

Though Sanggenon G (SanG) from root bark ofMorus albawas known to exhibit anti-oxidant and anti-depressant effects, its underlying mechanisms still remain unclear. Herein SanG reduced the viability of A549 and H1299 non-small lung cancer cells (NSCLCs). Also, SanG increased sub-G1 population via inhibition of cyclin D1, cyclin E, CDK2, CDK4 and Bcl-2, cleavages of poly (ADP-ribose) polymerase (PARP) and caspase-3 in A549 and H1299 cells. Of note, SanG effectively inhibited c-Myc expression by activating ribosomal protein L5 (RPL5) and reducing c-Myc stability even in the presence of cycloheximide and 20% serum in A549 cells. Furthermore, SanG enhanced the apoptotic effect with doxorubicin in A549 cells. Taken together, our results for the first time provide novel evidence that SanG suppresses proliferation and induces apoptosis via caspase-3 activation and RPL5 mediated inhibition of c-Myc with combinational potential with doxorubicin.

Automated summary

The study revealed that Sanggenon G (SanG) can inhibit the viability of non-small lung cancer cells through multiple pathways, including inhibition of cyclins and apoptosis-related proteins. Additionally, SanG can induce apoptosis by activating caspase-3 and RPL5, showing potential for combination with other drugs.