RED RICE BRAN EXTRACT SUPPRESSES COLON CANCER CELLS VIA APOPTOSIS INDUCTION/CELL CYCLE ARREST AND EXERTS ANTIMUTAGENIC ACTIVITY.

Ratsada Praphasawat, Sarawoot Palipoch, Prasit Suwannalert, Witchuda Payuhakrit, Paween Kunsorn, Sarunya Laovitthayanggoon, Sinittra Thakaew, Narongsuk Munkong, Warangkhana Klajing
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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.

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红米糠提取物通过细胞凋亡诱导/细胞周期阻滞抑制结肠癌细胞并发挥抗突变活性。
背景:红米糠提取物(RRBE)含有多种生物活性物质,具有抗氧化和抗炎作用。目的:评价RRBE在人结肠癌癌症细胞中的抗癌潜力及其对非癌细胞的诱变/抗突变作用。材料和方法:用台盼蓝排斥法测定RRBE对HCT116、HT29细胞系和非癌性HEK293细胞系的细胞毒作用,并用MTS和集落形成法测定其抗增殖作用。使用ELISA评估细胞凋亡诱导,并通过流式细胞术评估细胞凋亡率和细胞周期进展。通过V79细胞系微核试验分析RRBE的诱变/抗诱变潜力。结果:RRBE导致结肠癌癌症细胞的细胞活力呈剂量依赖性降低,对HEK293细胞的细胞毒性有限。RRBE处理抑制了HCT116和HT29细胞的增殖,并诱导了细胞凋亡,这可以通过增加的DNA片段和凋亡细胞计数来证明。此外,RRBE治疗显著增加了G2/M期的细胞数量,从而触发了结肠癌细胞中细胞周期的阻滞。有趣的是,RRBE并没有增加V79细胞的微核发生率,但减少了由mitomycin C引起的微核形成。结论:RRBE在体外具有非致突变性和抗突变作用的同时,有效地抑制了人结肠癌癌症细胞的增殖,诱导了细胞凋亡,并引起了细胞周期阻滞。
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