机译:通过下调CMTM4并激活PI3K / AKT途径来促进胰腺星状细胞衍生出ExosoMal MiR-5703的胰腺癌
Peking Univ First Hosp Dept Gen Surg Beijing 100034 Peoples R China;
Zhengzhou Univ Dept Hepatopancreatobiliary Surg Affiliated Hosp 1 Zhengzhou 450052 Peoples R;
Peking Univ First Hosp Dept Gen Surg Beijing 100034 Peoples R China;
Peking Univ First Hosp Dept Gen Surg Beijing 100034 Peoples R China;
Univ Ulm Clin Gen Visceral &
Transplantat Surg D-89081 Ulm Germany;
Peking Univ First Hosp Dept Gen Surg Beijing 100034 Peoples R China;
Peking Univ First Hosp Dept Gen Surg Beijing 100034 Peoples R China;
Pancreatic cancer; PSCs; Exosomal miR-5703; CMTM4; PAK4;
机译:源自胰腺星状细胞的外泌体miR-5703通过下调CMTM4促进胰腺癌生长
机译:来自胰星形细胞的NGF通过PI3K / AKT / GSK信号通路诱导胰腺癌增殖和侵袭
机译:Saikosaponin D通过PI3K / AKT / MTOR途径抑制胰腺星状细胞的自噬改善胰腺纤维化
机译:胰腺星状细胞活化伴有胰腺星状细胞活化,伴有秘密的变化
机译:胰腺星状细胞与胰腺癌肿瘤之间的相互作用
机译:来自胰腺星状细胞的NGF通过PI3K / AKT / GSK信号途径诱导胰腺癌的增殖和侵袭
机译:在胰腺星状细胞中的外泌体microRNA-21上调促进胰腺癌细胞迁移,增强RAS / ERK途径活动
机译:分子靶向pI3K / akt通路预防激素抵抗前列腺癌的发生