Targeting the HECTD3-p62 axis increases the radiosensitivity of triple negative breast cancer cells

KIZ OpenIR > 科研部门 > 肿瘤生物学（陈策实）

	Targeting the HECTD3-p62 axis increases the radiosensitivity of triple negative breast cancer cells
	Huang, MB; Liu, WJ; Cheng, Z; Li, FB; Kong, YJ; Yang, CY; Tang, Y; Jiang, DW; Li, WH; Hu, YD; Hu, JH; Puno, P; Chen, CS
	2024
发表期刊	CELL DEATH DISCOVERY
卷号	10 期号:1
摘要	Triple negative breast cancer is the most malignant subtype of breast cancer and current treatment options are limited. Radiotherapy is one of the primary therapeutic options for patients with TNBC. In this study, we discovered that the E3 ubiquitin ligase, HECTD3, promoted TNBC cell survival after irradiation. HECTD3 collaborated with UbcH5b to promote p62 ubiquitination and autophagy while HECTD3 deletion led to p62 accumulation in the nucleus in response to irradiation, thus inhibiting RNF168 mediated DNA damage repair. Furthermore, the HECTD3/UbcH5b inhibitor, PC3-15, increased the radiosensitivity of TNBC cells by inhibiting DNA damage repair. Taken together, we conclude that HECTD3 promotes autophagy and DNA damage repair in response to irradiation in a p62-denpendent manner, and that inhibition of the HECTD3-p62 axis could be a potential therapeutic strategy for patients with TNBC in addition to radiotherapy.
收录类别	SCI
语种	英语
文献类型	期刊论文
条目标识符	http://ir.kiz.ac.cn/handle/152453/14562
专题	科研部门_肿瘤生物学（陈策实）
推荐引用方式 GB/T 7714	Huang, MB,Liu, WJ,Cheng, Z,et al. Targeting the HECTD3-p62 axis increases the radiosensitivity of triple negative breast cancer cells[J]. CELL DEATH DISCOVERY,2024,10(1).
APA	Huang, MB.,Liu, WJ.,Cheng, Z.,Li, FB.,Kong, YJ.,...&Chen, CS.(2024).Targeting the HECTD3-p62 axis increases the radiosensitivity of triple negative breast cancer cells.CELL DEATH DISCOVERY,10(1).
MLA	Huang, MB,et al."Targeting the HECTD3-p62 axis increases the radiosensitivity of triple negative breast cancer cells".CELL DEATH DISCOVERY 10.1(2024).

条目包含的文件
文件名称/大小	文献类型	版本类型	开放类型	使用许可
CCS2025040707.pdf（9408KB）	期刊论文	出版稿	开放获取	CC BY-NC-SA	请求全文