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EMP1通过激活PI3K/AKT信号通路诱导胰腺癌细胞增殖和迁移

EMP1 Induces Proliferation and Migration of Pancreatic Cancer Cells by Activating PI3K/AKT Signaling Pathway

  • 摘要:
    目的 探讨EMP1在胰腺癌细胞中生物学作用及其促进肿瘤进展的相关分子机制。
    方法 通过慢病毒转染,获得稳定的EMP1敲低肿瘤细胞系。通过CCK-8、克隆形成实验检测EMP1对肿瘤细胞增殖的影响。通过划痕实验、Transwell实验检测EMP1对肿瘤细胞迁移、侵袭的影响。通过Western blot探究EMP1对下游信号通路的影响。
    结果 qRT-PCR和Western blot结果显示EMP1在胰腺癌细胞中高表达。CCK-8、克隆形成、划痕和Transwell实验结果表明EMP1在胰腺癌中促进癌细胞增殖、迁移及侵袭。Western blot实验结果发现EMP1可能是通过PI3K/AKT促进肿瘤进展。
    结论 本研究表明EMP1可能激活PI3K/AKT信号通路促进胰腺癌细胞增殖、迁移与侵袭,从而正向调控肿瘤进展。

     

    Abstract:
    Objective To investigate the biological behavior of EMP1 in pancreatic cancer cells and the molecular mechanism of EMP1 in promoting tumor progression.
    Methods A stable EMP1 knockdown cell line was obtained by lentivirus transfection. The effect of EMP1 on the proliferation of cancer cells was determined by CCK-8 and clonal formation assay. The effect of EMP1 on the migration and invasion of cancer cells was detected by scratch test and Transwell test. The influence of EMP1 on downstream signaling pathways was investigated by Western blot.
    Results The results of qRT-PCR and Western blot showed that EMP1 was highly expressed in pancreatic cancer cells. The results of CCK-8, colony formation, scratch, and Transwell assays indicated that EMP1 promoted the proliferation, migration, and invasion of pancreatic cancer cells. Western blot results revealed that EMP1 might promote tumor progression through the PI3K/AKT signaling pathway.
    Conclusion This study suggested that EMP1 may activate the PI3K/AKT signaling pathway to promote the proliferation, migration, and invasion of pancreatic cancer cells, thereby positively regulating tumor progression.

     

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