Enhancement of TRAIL-induced apoptosis by 5-fluorouracil requires activating Bax and p53 pathways in TRAIL-resistant lung cancers
Metrics: PDF 970 views | HTML 1334 views | ?
Uddin MD. Nazim1, Mohammad Rasheduzzaman1, You-Jin Lee1, Dai-Wu Seol2, Sang-Youel Park1
1Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk 54596, Republic of Korea
2Faculty of Pharmacy, Chung-Ang University School of Pharmacy, Seoul 156-756, Republic of Korea
Sang-Youel Park, email: firstname.lastname@example.org
Keywords: 5-fluorouracil, TRAIL, apoptosis, lung cancer cells
Received: August 01, 2016 Accepted: January 03, 2017 Published: February 02, 2017
Lung cancer, especially lung adenocarcinoma, is one of the main causes of death worldwide. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a primary anticancer agent and a member of the tumor necrosis factor family that selectively induces apoptosis in various tumor cells, but not in normal cells. Combination chemotherapy can be used for treating specific cancer types even at progressive stages. In the present study, we observed that 5-fluorouracil, which exerts anticancer effects by inhibiting tumor cell proliferation, enhanced TRAIL-induced apoptosis of TRAIL-resistant human adenocarcinoma A549 cells. Interestingly, 5-fluorouracil treatment markedly increased Bax and p53 levels and 5-fluorouracil and TRAIL cotreatment increased Ac-cas3 and Ac-cas8 levels compared with those in control cells. Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.