Abstract
Increasing the effectiveness and reliability of Akt inhibition in lung cancer treatment may pave the way for a more favorable use of this method in the future. Therefore, we aimed to evaluate the possible role of RhoB in the regulation of Akt inhibition in NSCLC. The study was conducted using the NSCLC cell line A549. Small interfering RNA (siRNA)-mediated RhoB knockdown was performed and combined with perifosine (Akt inhibitor) treatment. Cell proliferation was detected by xCELLigence® RTCA. RhoB, pAkt, and Bcl2l11 expressions were analyzed by ELISA. Apoptosis rates were determined by flow cytometry. We knocked down RhoB in A549 cells using siRNA. According to the results of the 72-hour experiment, RhoB upregulation was observed to reduce the antiproliferative ac-tivity of the Akt inhibitor. The pAkt level was significantly lower in the group where the Akt inhibitor was applied to RhoB-silenced cells via siRNA compared to other treatment groups. The percentage of apoptosis in the group where the Akt inhibitor was applied to RhoB-silenced cells was found to be significantly higher than in the RhoB-suppressed group. Both proliferation and apoptosis tests determined that the RhoB molecule is a negative regulator of the anti-tumor activity of Akt inhibition in non-small cell lung cancer. This study suggests that RhoB expression may play a critical role in the regulation of Akt inhibition in NSCLC, potentially opening new avenues for treatment strategies.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call