YBX1 as an oncogenic factor in T-cell acute lymphoblastic leukemia

作者全名："Li, Huan; Zhang, Danlan; Fu, Qiuxia; Wang, Shang; Wang, Zhongyuan; Zhang, Xin; Chen, Xin; Zhu, Xiaoyu; An, Na; Chen, Yun; Zhou, Liang; Lu, Desheng; Zhao, Na"

作者地址："[Li, Huan; Zhang, Danlan; Fu, Qiuxia; Wang, Zhongyuan; Zhang, Xin; Chen, Xin; An, Na; Zhou, Liang; Lu, Desheng] Shenzhen Univ Med Sch, Int Canc Ctr, Dept Pharmacol, Guangdong Prov Key Lab Reg Immun & Dis,Marshall La, Shenzhen, Peoples R China; [Wang, Shang] Chongqing Med Univ, Coll Tradit Chinese Med, Chongqing Key Lab Tradit Chinese Med Prevent & Cur, Chongqing, Peoples R China; [Zhu, Xiaoyu; Zhao, Na] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Hematol, Div Life Sci & Med, Hefei, Peoples R China; [Chen, Yun] Nanjing Med Univ, Gusu Sch, Dept Immunol, Key Lab Human Funct Genom Jiangsu Prov, Nanjing, Peoples R China; [Zhao, Na] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Hematol, Div Life Sci & Med, Lujiang Rd 17, Hefei 230001, Peoples R China"

通信作者："Zhao, N (通讯作者)，Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Hematol, Div Life Sci & Med, Lujiang Rd 17, Hefei 230001, Peoples R China."

来源：BLOOD ADVANCES

ESI学科分类：　

WOS号：WOS:001076365700001

JCR分区：Q1

影响因子：7.4

年份：2023

卷号：7

期号：17

开始页：4874

结束页：4885

文献类型：Article

关键词：YBX1 is required for survival in T-ALL by augmenting leukemia cell viability and cell cycle progression and inhibiting cell apoptosis.; YBX1 depletion impedes leukemogenesis in human T-ALL xenograft and NOTCH1-induced T-ALL model

摘要："Y-box-binding protein 1 (YBX1), a member of the RNA-binding protein family, is a critical regulator of cell survival in various solid tumors and acute myeloid leukemia. However, the function of YBX1 in T-cell acute lymphoblastic leukemia (T-ALL) remains elusive. Here, we found that YBX1 was upregulated in patients with T-ALL, T-ALL cell lines, and NOTCH1induced T-ALL mice. Furthermore, depletion of YBX1 dramatically reduced cell proliferation, induced cell apoptosis, and induced G0/G1 phase arrest in vitro. Moreover, YBX1 depletion significantly decreased the leukemia burden in the human T-ALL xenograft and NOTCH1-induced T-ALL mice model in vivo. Mechanistically, downregulation of YBX1 markedly inhibited the expression of total AKT serine/threonine kinase (AKT), p-AKT, total extracellular signal-regulated kinase (ERK), and p-ERK in T-ALL cells. Taken together, our results uncovered a critical role of YBX1 in the leukemogenesis of T-ALL, which may have great potential as a biomarker and therapeutic target in T-ALL."

基金机构：National Natural Science Foun-dation of China [31970739]; Anhui Natural Science Founda-tion [2108085QH322]

基金资助正文：Acknowledgments This research was funded by the National Natural Science Foun-dation of China (31970739) and Anhui Natural Science Founda-tion (2108085QH322) .