Vorinostat enhances the therapeutic potential of Erlotinib via MAPK in lung cancer cells

Cancer Treatment and Research Communications

Fatma Al-Mulhim¹  Amany I Alqosaibi²  Shaimaa Abdel-Ghany³  Hussein Sabit³ 

[1] Breast Imaging Division, KFHU, Imam Abdulrahman Bin Faisal University, Saudi Arabia;Department of Biology, College of Science, Imam Abdulrahman Bin Faisal University, Dammam, P. O. 4 Box 1982, Saudi Arabia;Department of Environmental Biotechnology, College of Biotechnology, Misr University for Science and Technology, Giza, Egypt;

关键词: Lung cancer;    Erlotinib;    ERL;    SAHA;    Vorinostat;    MAPK;   

DOI  :  

来源: DOAJ

【 摘 要 】

Background: Lung cancer is the second most common cancer in both men and women, with an estimated 235,760 new cases and 131,880 deaths in 2021 in the US. Despite the modern therapies being available such as radiotherapy and chemotherapy, death rates are still increasing. Erlotinib (ERL) is one of the treatment options for lung cancer, although the probability for the patients to develop resistance to ERL constrains its reliability. The aim of the present study is to assess the synergetic effect of combining ERL with vorinostat (SAHA) on the progression of lung cancer cells. Results: Adenocarcinoma alveolar basal epithelial cells (A549) were treated with either ERL, SAHA as mono drugs or with the combination of them for 24 h. Cytotoxicity assay and cell cycle analysis along with apoptosis detection were investigated. The expression profile of CDH1, TGF1, and MAPK was also assessed. Results showed an elevation in the apoptosis level in all treatments compared to WISH; the normal human amnion-derived cells. Furthermore, the treatments caused the cell cycle to arrest at G2/M, indicating its cytotoxic activity. Conclusion: The combination of SAHA and ERL significantly increased the level of apoptosis in lung cancer cells. Meanwhile, this combination treatment downregulated MAPK compared to the mono drugs and the control cells, suggesting the potential role of MAPK in regulating apoptosis and cell cycle machinery in lung cancer.

【 授权许可】

Unknown