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甜茶中的根皮苷通过拮抗 JAK2/STAT3 信号通路抑制食管癌的进展。

Phlorizin from sweet tea inhibits the progress of esophageal cancer by antagonizing the JAK2/STAT3 signaling pathway.

机构信息

School of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.

College of Life Science, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.

出版信息

Oncol Rep. 2021 Jul;46(1). doi: 10.3892/or.2021.8088. Epub 2021 May 26.

DOI:10.3892/or.2021.8088
PMID:34036398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8165578/
Abstract

Phlorizin, an important member of the dihydrochalcone family, has been widely used as a Chinese Traditional Medicine for treatment of numerous diseases. The present study aimed to investigate the potential therapeutic effects of phlorizin on esophageal cancer. Phlorizin, extracted from sweet tea, was used to treat esophageal cancer cells. Cell proliferation, migration and invasion were determined using Cell Counting Kit‑8 and colony formation assays, and wound healing and Transwell assays, respectively. RNA sequencing and bioinformatics analysis was used to investigate the potential mechanism of phlorizin in the development of esophageal cancer. Fluorescent staining and flow cytometry was used to measure the level of apoptosis. The expression level of the proteins, P62/SQSTM1 and LC3 І/II, and the effect of phlorizin on the JAK2/STAT3 signaling pathway was detected using western blot analysis. The results demonstrated that phlorizin could inhibit cell proliferation, migration and invasion. Bioinformatics analysis showed that phlorizin might be involved in pleiotropic effects, such as the 'JAK/STAT signaling pathway' (hsa04630), 'MAPK signaling pathway'(hsa04010) and 'apoptosis' (hsa04210). It was also confirmed that phlorizin promoted apoptosis and inhibited autophagy in the esophageal cancer cells. Notably, phlorizin might inhibit the proteins in the JAK/STAT signaling pathway, which would affect cancer cells. Taken together, the present data showed that phlorizin inhibited the progression of esophageal cancer by antagonizing the JAK2/STAT3 signaling pathway.

摘要

根皮苷是二氢查尔酮家族的重要成员,已被广泛用作治疗多种疾病的中药。本研究旨在探讨根皮苷对食管癌的潜在治疗作用。从甜茶中提取的根皮苷用于治疗食管癌细胞。使用细胞计数试剂盒-8 和集落形成实验分别测定细胞增殖、迁移和侵袭,使用划痕愈合和 Transwell 实验分别测定细胞迁移和侵袭。通过 RNA 测序和生物信息学分析研究根皮苷在食管癌发生发展中的潜在作用机制。荧光染色和流式细胞术用于测量细胞凋亡水平。通过 Western blot 分析检测蛋白质 P62/SQSTM1 和 LC3 Ⅰ/Ⅱ的表达水平以及根皮苷对 JAK2/STAT3 信号通路的影响。结果表明,根皮苷可抑制细胞增殖、迁移和侵袭。生物信息学分析表明,根皮苷可能参与多种效应,如“JAK/STAT 信号通路”(hsa04630)、“MAPK 信号通路”(hsa04010)和“细胞凋亡”(hsa04210)。还证实根皮苷可促进食管癌细胞凋亡并抑制自噬。值得注意的是,根皮苷可能抑制 JAK/STAT 信号通路中的蛋白质,从而影响癌细胞。综上所述,本研究数据表明,根皮苷通过拮抗 JAK2/STAT3 信号通路抑制食管癌的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/72632dc11403/or-46-01-8088-g07.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/69304cbda47e/or-46-01-8088-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/72632dc11403/or-46-01-8088-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/673de929a265/or-46-01-8088-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/1aa6f84b2b9b/or-46-01-8088-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/7972fa184ef2/or-46-01-8088-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/2fee895df473/or-46-01-8088-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/74a07e1d8378/or-46-01-8088-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/2330a4b4066a/or-46-01-8088-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/69304cbda47e/or-46-01-8088-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e25/8165578/72632dc11403/or-46-01-8088-g07.jpg

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