B7-H3 suppresses doxorubicin-induced senescence-like growth arrest in colorectal cancer through the AKT/TM4SF1/SIRT1 pathway

被引：39
作者：
Wang, Ruoqin [1 ,2 ,3 ,4 ]
Sun, Linqing [2 ]
Xia, Suhua [5 ]
Wu, Hongya [6 ]
Ma, Yanchao [1 ,2 ]
Zhan, Shenghua [1 ]
Zhang, Guangbo [1 ,3 ]
Zhang, Xueguang [1 ,3 ,6 ]
Shi, Tongguo [1 ,3 ,4 ]
Chen, Weichang [1 ,2 ,3 ,4 ,6 ]
机构：
[1] Soochow Univ, Jiangsu Inst Clin Immunol, Affiliated Hosp 1, 708 Renmin Rd, Suzhou, Peoples R China
[2] Soochow Univ, Dept Gastroenterol, Affiliated Hosp 1, 188 Shizi Rd, Suzhou, Peoples R China
[3] Soochow Univ, Jiangsu Key Lab Clin Immunol, 708 Renmin Rd, Suzhou, Peoples R China
[4] Soochow Univ, Suzhou Key Lab Tumor Immunol Digest Tract, Affiliated Hosp 1, 708 Renmin Rd, Suzhou, Peoples R China
[5] Soochow Univ, Dept Oncol, Affiliated Hosp 1, 188 Shizi Rd, Suzhou, Peoples R China
[6] Soochow Univ, Jiangsu Key Lab Gastrointestinal Tumor Immunol, Affiliated Hosp 1, 708 Renmin Rd, Suzhou, Peoples R China
来源：
CELL DEATH & DISEASE | 2021年 / 12卷 / 05期
基金：
中国国家自然科学基金;
关键词：
HUMAN PROSTATE-CANCER; CELLULAR SENESCENCE; SECRETORY PHENOTYPE; BREAST-CANCER; CELLS; APOPTOSIS; SIRT1; EXPRESSION; SURVIVAL; TM4SF1;
D O I：
10.1038/s41419-021-03736-2
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Emerging evidence suggests that cellular senescence induced by chemotherapy has been recognized as a new weapon for cancer therapy. This study aimed to research novel functions of B7-H3 in cellular senescence induced by a low dose of doxorubicin (DOX) in colorectal cancer (CRC). Here, our results demonstrated that B7-H3 knockdown promoted, while B7-H3 overexpression inhibited, DOX-induced cellular senescence. B7-H3 knockdown dramatically enhanced the growth arrest of CRC cells after low-dose DOX treatment, but B7-H3 overexpression had the opposite effect. By RNA-seq analysis and western blot, we showed that B7-H3 prevented cellular senescence and growth arrest through the AKT/TM4SF1/SIRT1 pathway. Blocking the AKT/TM4SF1/SIRT1 pathway dramatically reversed B7-H3-induced resistance to cellular senescence. More importantly, B7-H3 inhibited DOX-induced cellular senescence of CRC cells in vivo. Therefore, targeting B7-H3 or the B7-H3/AKT/TM4SF1/SIRT1 pathway might be a new strategy for promoting cellular senescence-like growth arrest during drug treatment in CRC.
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页数：17
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