Ali Flores-Pérez1, Laurence A Marchat2,3, Lidia López Sánchez1, Diana Romero-Zamora1, Elena Arechaga-Ocampo4, Nayeli Ramírez-Torres1, José Díaz Chávez5, Ángeles Carlos-Reyes6, Horacio Astudillo-de la Vega7, Erika Ruiz-García8, Abrahan González-Pérez1, César López-Camarillo1. 1. Genomics Sciences Program, Autonomous University of Mexico City, Mexico City, Mexico. 2. Molecular Biomedicine Program, National School of Medicine and Homeopathy, National Polytechnic Institute, Mexico. 3. Biotechnology Program, National School of Medicine and Homeopathy, National Polytechnic Institute, Mexico. 4. Natural Sciences Department, Metropolitan Autonomous University, Mexico. 5. Oncogenomics Laboratory, National Institute of Cancerology, Mexico. 6. Lung Cancer Laboratory, National Institute of Respiratory Diseases, Mexico. 7. Laboratory of Translational Cancer Research and Cellular Therapy, Oncology Hospital, Medical Center Siglo XXI, Mexico. 8. Translational Medicine Laboratory, National Institute of Cancerology, Mexico.
Abstract
PURPOSE: To search for regulated proteins in response to green tea (-)-epigallocatechin-3-gallate (EGCG) in A549 lung cancer cells. EXPERIMENTAL DESIGN: 2DE and ESI/multistage MS (ESI-MS/MS) were performed to identify modulated proteins in A549 cells treated with EGCG. Cell migration was evaluated by transwell assays. RNA interference was used to silence the hepatoma-derived growth factor (HDGF). Caspase-3, caspase-9, and HDGF were immunodetected by Western blot assays. Flow cytometry was used for detection of mitochondrial membrane potential and apoptosis. RESULTS: We found that HDGF expression was threefold suppressed by EGCG treatment. Downregulation of HDGF by EGCG was confirmed using anti-HDGF antibodies in three lung cancer cell lines. EGCG treatment and HDGF abrogation by RNA interference resulted in a decreased migration of A549 cells. In addition, EGCG induced a marked synergistic effect with cisplatin in cell death. Consistently, an enhanced cytotoxicity in HDGF-silenced cells was also found. Cell death was associated to increased apoptosis, disruption of the mitochondrial membrane potential, and activation of caspase-3 and caspase-9. CONCLUSION AND CLINICAL RELEVANCE: Our data suggest for the first time that abrogation of HDGF by EGCG enhances cisplatin-induced apoptosis and sensitize A549 cells to chemotherapy. Therefore, we propose that decreasing the HDGF levels by using EGCG may represent a novel strategy in lung cancer therapy.
PURPOSE: To search for regulated proteins in response to green tea (-)-epigallocatechin-3-gallate (EGCG) in A549 lung cancer cells. EXPERIMENTAL DESIGN: 2DE and ESI/multistage MS (ESI-MS/MS) were performed to identify modulated proteins in A549 cells treated with EGCG. Cell migration was evaluated by transwell assays. RNA interference was used to silence the hepatoma-derived growth factor (HDGF). Caspase-3, caspase-9, and HDGF were immunodetected by Western blot assays. Flow cytometry was used for detection of mitochondrial membrane potential and apoptosis. RESULTS: We found that HDGF expression was threefold suppressed by EGCG treatment. Downregulation of HDGF by EGCG was confirmed using anti-HDGF antibodies in three lung cancer cell lines. EGCG treatment and HDGF abrogation by RNA interference resulted in a decreased migration of A549 cells. In addition, EGCG induced a marked synergistic effect with cisplatin in cell death. Consistently, an enhanced cytotoxicity in HDGF-silenced cells was also found. Cell death was associated to increased apoptosis, disruption of the mitochondrial membrane potential, and activation of caspase-3 and caspase-9. CONCLUSION AND CLINICAL RELEVANCE: Our data suggest for the first time that abrogation of HDGF by EGCG enhances cisplatin-induced apoptosis and sensitize A549 cells to chemotherapy. Therefore, we propose that decreasing the HDGF levels by using EGCG may represent a novel strategy in lung cancer therapy.
Authors: Alessandra Vidotto; Giovana M Polachini; Marina de Paula-Silva; Sonia M Oliani; Tiago Henrique; Rossana V M López; Patrícia M Cury; Fabio D Nunes; José F Góis-Filho; Marcos B de Carvalho; Andréia M Leopoldino; Eloiza H Tajara Journal: BMC Med Genomics Date: 2018-08-29 Impact factor: 3.063
Authors: Wamidh H Talib; Dima Awajan; Reem Ali Hamed; Aya O Azzam; Asma Ismail Mahmod; Intisar Hadi Al-Yasari Journal: Molecules Date: 2022-08-25 Impact factor: 4.927