期刊,中华医学杂志（英文版） 2024年卷2期_国家学术搜索

期刊信息/Journal information

中华医学杂志（英文版）

中华医学会

主办单位：中华医学会

主　　编：照日格图

出版周期：半月刊

国际刊号：0366-6999

电子邮箱：renlihua@cma.org.cn

电　　话：010-85158321

邮政编码：100710

地　　址：北京市东城区东四西大街42号

中华医学杂志（英文版）/Journal Chinese Medical JournalCSCDCSTPCD北大核心SCI

查看更多>>1887年创刊，中华医学会主办。中华医学杂志英文版(Chinese Medical Journal)是中华医学会会刊，是中国惟一被SCI核心版收录、具有百年以上历史的医学期刊。重点报道我国医学各学科最新进展和高水平科研成果，目前已被《科学引文索引（SCI）》、《医学索引（IM）》、Medline等国际著名检索系统收录。2009年SCI影响因子0.952，SCI被引频次3407。2010年被国际医学期刊编辑委员会（ICMJE）吸收为新成员。多次获得国家期刊奖、科协专项基金、自然基金等奖项和资助。实行全文上网（），网上投稿审稿()。

正式出版

收录年代

Cell softness reveals tumorigenic potential via ITGB8/AKT/glycolysis signaling in a mice model of orthotopic bladder cancer

Shi QiuYaqi QiuLinghui DengLing Nie...

209-221页

查看更多>>摘要：Background:Bladder cancer,characterized by a high potential of tumor recurrence,has high lifelong monitoring and treatment costs.To date,tumor cells with intrinsic softness have been identified to function as cancer stem cells in several cancer types.Nonetheless,the existence of soft tumor cells in bladder tumors remains elusive.Thus,our study aimed to develop a micro-barrier microfluidic chip to efficiently isolate deformable tumor cells from distinct types of bladder cancer cells.Methods:The stiffness of bladder cancer cells was determined by atomic force microscopy(AFM).The modified microfluidic chip was utilized to separate soft cells,and the 3D Matrigel culture system was to maintain the softness of tumor cells.Expression patterns of integrinβ8(ITGB8),protein kinase B(AKT),and mammalian target of rapamycin(mTOR)were determined by Western blotting.Double immunostaining was conducted to examine the interaction between F-actin and tripartite motif containing 59(TRIM59).The stem-cell-like characteristics of soft cells were explored by colony formation assay and in vivo studies upon xenografted tumor models.Results:Using our newly designed microfluidic approach,we identified a small fraction of soft tumor cells in bladder cancer cells.More importantly,the existence of soft tumor cells was confirmed in clinical human bladder cancer specimens,in which the number of soft tumor cells was associated with tumor relapse.Furthermore,we demonstrated that the biomechanical stimuli arising from 3D Matrigel activated the F-actin/ITGB8/TRIM59/AKT/mTOR/glycolysis pathways to enhance the softness and tumorigenic capacity of tumor cells.Simultaneously,we detected a remarkable up-regulation in ITGB8,TRIM59,and phospho-AKT in clinical bladder recurrent tumors compared with their non-recurrent counterparts.Conclusions:The ITGB8/TRIM59/AKT/mTOR/glycolysis axis plays a crucial role in modulating tumor softness and sternness.Meanwhile,the soft tumor cells become more sensitive to chemotherapy after stiffening,that offers new insights for hampering tumor progression and recurrence.

原文链接:

国家科技期刊平台
NETL
NSTL
万方数据

AZD1775 and anti-PD-1 antibody synergistically sensitize hepatoma to radiotherapy

Yichun YinJian WangJunxuan YKaiyue Zhang...

222-231页

查看更多>>摘要：Background:Radiation(IR)-induced DNA damage triggers cell cycle arrest and has a suppressive effect on the tumor microenvi-ronment(TME).Wee1,a cell cycle regulator,can eliminate G2/M arrest by phosphorylating cyclin-dependent kinase 1(CDK1).Meanwhile,programed death-1/programed death ligand-1(PD-1/PDL-1)blockade is closely related to TME.This study aims to investigate the effects and mechanisms of Wee1 inhibitor AZD1775 and anti-PD-1 antibody(anti-PD-1 Ab)on radiosensitization of hepatoma.Methods:The anti-tumor activity of AZD1775 and IR was determined by 3-(4,5-dimethylthiazol-2-y1)-2,5-diphenyltetrazolium bromide(MTT)assay on human and mouse hepatoma cells HepG2,Hepa1-6,and H22.The anti-hepatoma mechanism of AZD1775 and IR revealed by flow cytometry and Western blot in vitro.A hepatoma subcutaneous xenograft mice model was con-structed on Balb/c mice,which were divided into control group,IR group,AZD1775 group,IR+AZD1775 group,IR+anti-PD-1 Ab group,and the IR+AZD1775+anti-PD-1 Ab group.Cytotoxic CD8+T cells in TME were analyzed by flow cytometry.Results:Combining IR with AZD1775 synergistically reduced the viability of hepatoma cells in vitro.AZD1775 exhibited antitu-mor effects by decreasing CDK1 phosphorylation to reverse the IR-induced G2/M arrest and increasing IR-induced DNA damage.AZD1775 treatment also reduced the proportion of PD-1+/CD8+T cells in the spleen of hepatoma subcutaneous xenograft mice.Further studies revealed that AZD1775 and anti-PD-1 Ab could enhance the radiosensitivity of hepatoma by enhancing the levels of interferon y(IFNγ)+or Ki67+CD8 T cells and decreasing the levels of CD8+Tregs cells in the tumor and spleen of the hepatoma mice model,indicating that the improvement of TME was manifested by increasing the cytotoxic factor IFNγ expression,enhanc-ing CD8+T cells proliferation,and weakening CD8+T cells depletion.Conclusions:This work suggests that AZD1775 and anti-PD-1 Ab synergistically sensitize hepatoma to radiotherapy by enhanc-ing IR-induced DNA damage and improving cytotoxic CD8+T cells in TME.

原文链接: