Linderalactone inhibits human lung cancer growth by modulating the expression of apoptosis-related proteins, G2/M cell cycle arrest and inhibition of JAK/STAT signalling pathway

Purpose: The main purpose of the current research work was to evaluate the antitumor effects of linderalactone in A-549 human lung carcinoma cell line along with the study its effects on apoptosis-related proteins, cell cycle phase distribution and JAK/STAT signalling pathway.

Methods: The viability of lung Cancer cell line was investigated by MTT assay at varying doses of linderalactone. Apoptosis was detected by using fluorescence microscopy and flow cytometry. Cell cycle analysis was carried out by flow cytometery. The protein expression was examined by western blotting.

Results: Linderalactone could inhibit the proliferation of the lung Cancer A-549 cells with an IC50 of 15 µM. Further investigations indicated the antiproliferative effects of linderalactone are due to Apoptosis induction which was further confirmed by Bax and Bcl-2 expression. It also induced G2/M cell cycle arrest which was also associated with alteration of the expression of several important proteins. Furthermore, linderalactone could also suppress the JAK/STAT signalling pathway.

Conclusions: In conclusion, linderalactone could be developed as a potential drug candidate against lung Cancer provided that further in depth studies are carried out in this direction focusing on its in vivo efficacy.