KrasG12D-LOH通过mTOR信号通路调控胰腺癌细胞的生物学行为
KrasG12D-LOH regulated biological behavior of Pancreatic cancer cells via mTOR signaling pathway
目的 观察KrasG12D-LOH对胰腺癌细胞生物学行为的影响及其相关作用机制。方法 从KrasG12D转基因胰腺导管腺癌小鼠的胰腺肿瘤组织中提取并筛选出KrasG12D细胞株和KrasG12D-LOH细胞株作为研究对象。分别在常规及缺氧条件下培养, 通过CCK-8细胞增殖实验、平板克隆形成实验和侵袭实验，研究KrasG12D-LOH对胰腺癌细胞在常氧及缺氧状态下增殖和侵袭转移能力的影响。应用Western blot检测mTOR信号通路相关蛋白表达的影响。结果 分别在常规及缺氧培养条件下，CCK-8实验和平板克隆形成实验检测结果显示KrasG12D-LOH细胞的增殖能力高于KrasG12D细胞。Transwell小室检测表明KrasG12D-LOH细胞的侵袭转移能力较强。与KrasG12D细胞相比，KrasG12D-LOH细胞mTOR的活性更高。结论 KrasG12D-LOH对胰腺癌细胞的增殖和侵袭具有正性调控作用，其机制可能与上调mTOR有关。
im：To investigate the distinct biologic behavior by KrasG12D with allelic loss of wildtype Kras. In addition, we attempted to the regulatory mechanisms between LOH-KrasG12D and mTOR signaling pathway. Methods: The cell growth curve was drawn by cell counting kit-8 assay, colony forming cell (CFC) assay and transwell migration experiment were used to investigate the ability of cell proliferation and migration. The expression of mTOR upstream signaling pathway associated proteins were measured by Western blot analysis. Results：Compared with KrasG12D, LOH-KrasG12D can induce cell proliferation, promote migration capability. The activity of mTOR signaling pathway were affected by the loss of wide Kras allele. Conclusions：These data strongly suggest that KrasG12D-LOH has upregulation tumor activity via mTOR signaling pathway.
周玲娜、胡明玥、张诗瑶、申霞、常立功、付玉琪、黄培林
肿瘤学基础医学分子生物学
胰腺癌Kras突变杂合性缺失mTOR增殖、侵袭
PancreaticKrasG12DLoss of heterozygositymTORProliferation and invasion
周玲娜,胡明玥,张诗瑶,申霞,常立功,付玉琪,黄培林.KrasG12D-LOH通过mTOR信号通路调控胰腺癌细胞的生物学行为[EB/OL].(2016-05-20)[2025-05-23].http://www.paper.edu.cn/releasepaper/content/201605-830.点此复制
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