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Pomolic acid and its glucopyranose ester promote apoptosis through autophagy in HT-29 colon cancer cells.
World Journal of Gastrointestinal Oncology ( IF 2.5 ) Pub Date : 2023-10-15 , DOI: 10.4251/wjgo.v15.i10.1756
Li-Yan Liu 1, 2 , Teng-Hua Yu 3 , Tie-Song Liao 1 , Peng Xu 4 , Ying Wang 5 , Min Shi 4 , Bin Li 1
Affiliation  

BACKGROUND Colon cancer remains a leading cause of death globally. Pomolic acid (PA) can be separated from the ethyl acetate fraction of achyrocline satureioides. AIM To determine the effects of PA and its glucopyranose ester, pomolic acid-28-O-β-D-glucopyranosyl ester (PAO), on colon cancer HT-29 cells. METHODS 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide assay was used to measure cell viability. Apoptosis was detected via hoechst 33342 staining. PI single staining was identified by flow cytometry to determine the cycle and scratch assay was used to observe the migration of HT-29 cells. The levels of mRNA and proteins were evaluated by q polymerase chain reaction and western blotting, respectively. RESULTS PA and PAO considerably inhibited the growth of the HT-29 cell line in a time and dose-dependent manner. After the administration of PA and PAO for 24 and 48 h, cell apoptosis was significantly promoted and HT-29 cells were arrested in the G0/G1 stage. The Bax/Bcl2 ratio was also increased, which activated cysteinyl aspartate specific proteinase 3, leading to apoptosis; it also increased the expression of light chain 3 II/I and Beclin1, which activated autophagy and caused cell death. This in turn increased the expression of p62 to promote cell apoptosis, inhibiting the levels of signal transducer and activator of transcription 3 (STAT3) and p-STAT3, suppressing the level of Bcl2, and promoting cell. CONCLUSION Both PA and PAO provide novel therapeutic strategies for treating colorectal cancer.

中文翻译:

Pomolic Acid 及其吡喃葡萄糖酯通过自噬促进 HT-29 结肠癌细胞凋亡。

背景技术结肠癌仍然是全球死亡的主要原因。可以从 Achyrocline satureioides 的乙酸乙酯馏分中分离出 Pomolic Acid (PA)。目的探讨PA及其吡喃葡萄糖酯泊莫酸-28-O-β-D-吡喃葡萄糖酯(PAO)对结肠癌HT-29细胞的影响。方法采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑测定法测定细胞活力。通过 Hoechst 33342 染色检测细胞凋亡。流式细胞术鉴定PI单染以确定循环,划痕实验观察HT-29细胞的迁移情况。分别通过q聚合酶链式反应和蛋白质印迹评估mRNA和蛋白质的水平。结果 PA和PAO以时间和剂量依赖性方式显着抑制HT-29细胞系的生长。PA和PAO给药24和48 h后,细胞凋亡明显促进,HT-29细胞被阻滞在G0/G1期。Bax/Bcl2比值也增加,从而激活半胱氨酰天冬氨酸特异性蛋白酶3,导致细胞凋亡;它还增加了轻链 3 II/I 和 Beclin1 的表达,从而激活自噬并导致细胞死亡。进而增加p62的表达促进细胞凋亡,抑制信号转导和转录激活因子3(STAT3)和p-STAT3的水平,抑制Bcl2的水平,促进细胞凋亡。结论 PA和PAO都为治疗结直肠癌提供了新的治疗策略。
更新日期:2023-10-15
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