RED RICE BRAN EXTRACT SUPPRESSES COLON CANCER CELLS VIA APOPTOSIS INDUCTION/CELL CYCLE ARREST AND EXERTS ANTIMUTAGENIC ACTIVITY
Issued Date
2023-10-14
Resource Type
ISSN
18129269
Scopus ID
2-s2.0-85176589974
Pubmed ID
37824769
Journal Title
Experimental Oncology
Volume
45
Issue
2
Start Page
220
End Page
230
Rights Holder(s)
SCOPUS
Bibliographic Citation
Experimental Oncology Vol.45 No.2 (2023) , 220-230
Suggested Citation
Praphasawat R., Palipoch S., Suwannalert P., Payuhakrit W., Kunsorn P., Laovitthayanggoon S., Thakaew S., Munkong N., Klajing W. RED RICE BRAN EXTRACT SUPPRESSES COLON CANCER CELLS VIA APOPTOSIS INDUCTION/CELL CYCLE ARREST AND EXERTS ANTIMUTAGENIC ACTIVITY. Experimental Oncology Vol.45 No.2 (2023) , 220-230. 230. doi:10.15407/exp-oncology.2023.02.220 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/91129
Title
RED RICE BRAN EXTRACT SUPPRESSES COLON CANCER CELLS VIA APOPTOSIS INDUCTION/CELL CYCLE ARREST AND EXERTS ANTIMUTAGENIC ACTIVITY
Other Contributor(s)
Abstract
Background. Red rice bran extract (RRBE) contains many biologically active substances exerting antioxidant and anti-inflammatory effects. Aim. To evaluate the anticancer potential of RRBE in human colon cancer cells and its mutagenic/antimutagenic effects on nonmalignant cells. Materials and Methods. The cytotoxic effect of RRBE was determined by trypan blue exclusion in HCT116, HT29 cell lines and a non-cancerous HEK293 cell line, and its antiproliferative effect using MTS and colony formation assay. The apoptosis induction was evaluated using ELISA, and the apoptotic rate and cell cycle progression were assessed by flow cytometry. The mutagenic/antimutagenic potential of RRBE was analyzed by micronucleus assay in the V79 cell line. Results. RRBE caused a dose-dependent reduction of cell viability in colon cancer cells and showed a limited cytotoxicity against HEK293 cells. The treatment with RRBE suppressed proliferation of HCT116 and HT29 cells and induced apoptosis as evidenced by the increased DNA fragmentation and the apoptotic cell counts. Furthermore, RRBE treatment significantly increased the number of cells at the G2/M phase triggering the arrest of the cell cycle in colon cancer cells. Interestingly, RRBE did not increase the micronucleus frequency in V79 cells but reduced the micronucleus formation caused by mitomycin C. Conclusion. RRBE effectively suppressed proliferation, induced apoptosis, and caused a cell cycle arrest in human colon cancer cells while being non-mutagenic and exerting antimutagenic effects in vitro.