| Literature DB >> 35361247 |
Xiaoqing Sun1, Zhenyu He2, Ling Guo3, Caiqin Wang4, Chuyong Lin5, Liping Ye6, Xiaoqing Wang7, Yue Li5, Meisongzhu Yang8, Sailan Liu3, Xin Hua1, Wen Wen2, Chao Lin3, Zhiqing Long2, Wenwen Zhang2, Han Li9, Yunting Jian5, Ziyuan Zhu10, Xianqiu Wu11,12, Huanxin Lin13.
Abstract
Entities:
Year: 2022 PMID: 35361247 PMCID: PMC8969285 DOI: 10.1186/s13046-022-02322-4
Source DB: PubMed Journal: J Exp Clin Cancer Res ISSN: 0392-9078
Fig. 5ALG3 enhances radioresistance via regulation of TGFBR2 glycosylation. a Downshift of TGFBR2 bands in ALG3-sg cells was detected by Western blot. But not TGFBR1 bands (b) Representative immunofluorescence images of TGFBR2 expression level in cytoplasmic and membrane fractions. c A schematic model of different subtypes of N-glycans. The round spots are mannose, the square ones are acetylglucosamine, and the red spot is the initial of the N-glycosylation site, which is initiated by ALG3. d TGFBR2 band shift could be seen in ALG3-sg cells or cells treated by tunicamycin. And downregulation of ALG3 reduced the expression level of p-SMAD2. e Representative immunofluorescence images of p-SMAD2 expression level in cytoplasmic and nuclear fractions. Nuclear translocation of p-SMAD2 was significantly decreased in ALG3-sg and tunicamycin treatment groups. f The co-immunoprecipitation between TGFBR1 and TGFBR2, TGFBR1 and p-SMAD2 could be detected in ALG3-control group, but not tunicamycin treatment, and ALG3-sg groups. g TGFBR2 inhibitor (LY2109761) in ALG3-transduced cells decreased the surviving fraction of breast cancer cells after radiation treatment, which were detected by CCK-8 assays. Data were analyzed by two-way ANOVA. Each bar represents the mean ± SD of three independent experiments. h Inhibition of TGFBR2 in ALG3-transduced cells decreased the number of colonies after radiation treatment. i Inhibition of TGFBR2 in ALG3-transduced cells decreased the proportion of CD44+CD24− cells, which were detected by flow cytometry. “ns” no significance, *P < 0.05