Urolithin A induces cell cycle arrest and apoptosis by inhibiting Bcl-2, increasing p53-p21 proteins and reactive oxygen species production in colorectal cancer cells
| Autor: | Islam Rady, Mohammad S El-Wetidy, Mohamad Rady, Mansoor-Ali Vaali-Mohammed, Thamer Bin Traiki, Maha-Hamadien Abdulla, Hamed Helal, Khayal Al-Khayal, Rehan Ahmad |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Cell cycle checkpoint Cell Antineoplastic Agents Apoptosis Biochemistry 03 medical and health sciences 0302 clinical medicine Cell Line Tumor medicine Humans neoplasms Cell Proliferation chemistry.chemical_classification Reactive oxygen species Original Paper Cell Death Cell growth Caspase 3 Cancer Cell Biology Cell Cycle Checkpoints medicine.disease digestive system diseases Urolithin 030104 developmental biology medicine.anatomical_structure chemistry Proto-Oncogene Proteins c-bcl-2 Cell culture 030220 oncology & carcinogenesis Cancer research Tumor Suppressor Protein p53 Colorectal Neoplasms Reactive Oxygen Species |
| Zdroj: | Cell Stress Chaperones |
| Popis: | Colorectal cancer (CRC) is the second most common gastrointestinal cancer globally. Prevention of tumor cell proliferation and metastasis is vital for prolonging patient survival. Polyphenols provide a wide range of health benefits and prevention from cancer. In the gut, urolithins are the major metabolites of polyphenols. The objective of our study was to elucidate the molecular mechanism of the anticancer effect of urolithin A (UA) on colorectal cancer cells. UA was found to inhibit the cell proliferation of CRC cell lines in a dose-dependent and time-dependent manner in HT29, SW480, and SW620 cells. Exposure to UA resulted in cell cycle arrest in a dose-dependent manner along with alteration in the expression of cell cycle–related protein. Treatment of CRC cell lines with UA resulted in the induction of apoptosis. Treatment of HT29, SW480, and SW620 with UA resulted in increased expression of the pro-apoptotic proteins, p53 and p21. Similarly, UA treatment inhibited the anti-apoptotic protein expression of Bcl-2. Moreover, exposure of UA induced cytochrome c release and caspase activation. Furthermore, UA was found to generate reactive oxygen species (ROS) production in CRC cells. These findings indicate that UA possesses anticancer potential and may be used therapeutically for the treatment of CRC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12192-020-01189-8. |
| Databáze: | OpenAIRE |
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