Praphasawat Ratsada, Thakaew Sinittra, Rawangkan Anchalee, Thongboontho Rungthip, Sooksaen Pornchai, Laovittayangkoon Sarunya, Klajing Warangkhana, Jaengpromma Pongnared, Kunsorn Paween, Suwannalert Prasit, Payuhakrit Witchuda
Department of Pathology, School of Medicine, University of Phayao, Phayao, Thailand.
Division of Microbiology, School of Medical Sciences, University of Phayao, Phayao, Thailand.
World J Oncol. 2023 Aug;14(4):266-276. doi: 10.14740/wjon1602. Epub 2023 Aug 4.
() (Lam.) Hack. plays an important role in detoxification. However, its anticancer activity has not yet been elucidated. The aim of our study was to examine the suppressive proliferation, anti-migration and mutagenic/antimutagenic properties of . Moreover, we set out to determine the cellular mechanism underlying its antiproliferation.
To investigate 's anticancer ability, HCT116 and HT29 cell lines were treated with a water extract containing , and then the cell viability was examined using the trypan blue exclusion method which were compared to HEK293 (non-cancerous cells). The anticancer effects were investigated by MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) and colony formation assay. Apoptosis induction, cell cycle distribution, and migration abilities were assessed by cell death detection enzyme-linked immunoassay (ELISA), flow cytometry, and wound healing assay. Finally, the mutagenicity and antimutagenicity were evaluated using the micronucleus assay.
Treatment with caused a loss of cell viability in HCT116 and HT29 cells (not found in HEK293), which had an IC (half-maximal inhibitory concentration) of 1,156.2 and 1,207.0 µg/mL, respectively. We found that significantly inhibited the proliferative function of HCT116 and HT29 cells. To find the mechanism that exerts a suppressive proliferation effect on , we determined the DNA fragmentation and cell cycle distribution. We also found that treatment increased apoptosis and arrested of the cell cycle at G0/G1 remarkably when compared with the control group. Moreover, could decrease the migration of HCT116 and HT29 cancer cells. Finally, the treatment of did not induce micronucleus formation but did decrease the micronucleus frequency against mutagen-mitomycin C.
did not possess any toxicity (cytotoxic and mutagenic) but has the potential for anticancer activity against human colorectal cells by increasing apoptosis, which leads to the suppression of cell proliferation. also inhibits cell migration and exerts antimutagenicity, thereby suggesting that might be useful for colorectal cancer treatment.
（）（Lam.）Hack. 在解毒过程中发挥着重要作用。然而，其抗癌活性尚未得到阐明。我们研究的目的是检测（该植物）的增殖抑制、抗迁移以及诱变/抗诱变特性。此外，我们着手确定其抗增殖作用背后的细胞机制。
为研究（该植物）的抗癌能力，用含有（该植物提取物）的水提取物处理HCT116和HT29细胞系，然后使用台盼蓝排斥法检测细胞活力，并与HEK293（非癌细胞）进行比较。通过MTS（3 -（4,5 - 二甲基噻唑 - 2 - 基）- 5 -（3 - 羧甲氧基苯基）- 2 -（4 - 磺基苯基）- 2H - 四氮唑）和集落形成试验研究抗癌效果。通过细胞死亡检测酶联免疫吸附测定（ELISA）、流式细胞术和伤口愈合试验评估细胞凋亡诱导、细胞周期分布和迁移能力。最后，使用微核试验评估诱变和抗诱变作用。
用（该植物提取物）处理导致HCT116和HT29细胞（在HEK293细胞中未发现）的细胞活力丧失，其IC（半数最大抑制浓度）分别为1,156.2和1,207.0μg/mL。我们发现（该植物提取物）显著抑制HCT116和HT29细胞的增殖功能。为找出对（该植物提取物）发挥增殖抑制作用的机制，我们测定了DNA片段化和细胞周期分布。我们还发现，与对照组相比，用（该植物提取物）处理可显著增加细胞凋亡并使细胞周期停滞在G0/G1期。此外，（该植物提取物）可减少HCT116和HT29癌细胞的迁移。最后，用（该植物提取物）处理未诱导微核形成，但确实降低了针对诱变剂丝裂霉素C的微核频率。
（该植物提取物）不具有任何毒性（细胞毒性和诱变性），但具有通过增加细胞凋亡来对抗人结肠癌细胞的抗癌活性潜力，这导致细胞增殖受到抑制。（该植物提取物）还抑制细胞迁移并发挥抗诱变作用，因此表明（该植物提取物）可能对结直肠癌治疗有用。
