长链非编码 RNA TUG1 促进胰腺导管腺癌的存活并与吉西他滨耐药相关。
LncRNA TUG1 promoted viability and associated with gemcitabine resistant in pancreatic ductal adenocarcinoma.
机构信息
Department of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, China.
Department of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, China.
出版信息
J Pharmacol Sci. 2018 Jun;137(2):116-121. doi: 10.1016/j.jphs.2018.06.002. Epub 2018 Jun 7.
OBJECTIVE
To investigate the underlying mechanism of lncRNA TUG1 in pancreatic ductal adenocarcinoma (PDAC).
METHODS
The expression of TUG1 was defined by qRT-PCR. The apoptotic cells were detected by flow cytometry assay. The cell migration and invasion were measured by scratch assay and Transwell assay. The level of ERK pathway was detected using Western blot.
RESULTS
Compared with normal tissues and cells, the expression of TUG1 was up-regulated in pancreatic cancer tissue and cells. Meanwhile, knockdown of TUG1 could promote PDAC cells apoptosis and inhibit PDAC cells viability, migration and invasion. In addition, overexpression of TUG1 enhanced the gemcitabine chemoresistance of PDAC cells. Surprisingly, gemcitabine combined with SCH772984 (a suppressor of ERK pathway) could reverse the drug resistance resulted from overexpression of TUG1.
CONCLUSION
TUG1 promoted the viability of PDAC cells and enhanced its resistance of gemcitabine.
目的
研究长链非编码 RNA TUG1 在胰腺导管腺癌（PDAC）中的作用机制。
方法
通过 qRT-PCR 确定 TUG1 的表达。通过流式细胞术检测细胞凋亡。通过划痕实验和 Transwell 实验检测细胞迁移和侵袭。使用 Western blot 检测 ERK 通路水平。
结果
与正常组织和细胞相比，TUG1 在胰腺癌组织和细胞中表达上调。同时，敲低 TUG1 可促进 PDAC 细胞凋亡并抑制 PDAC 细胞活力、迁移和侵袭。此外，TUG1 的过表达增强了 PDAC 细胞对吉西他滨的耐药性。令人惊讶的是，吉西他滨联合 SCH772984（ERK 通路的抑制剂）可逆转 TUG1 过表达引起的药物耐药性。
结论
TUG1 促进了 PDAC 细胞的活力，并增强了其对吉西他滨的耐药性。
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