Journal of Surgery Concepts & Practice ›› 2020, Vol. 25 ›› Issue (06): 486-492.doi: 10.16139/j.1007-9610.2020.06.009

• Original article • Previous Articles     Next Articles

Forkhead box D1 promotes invasion and metastasis of pancreatic cancer via extracellular signal-regulated kinase pathway

DING Fangmi, LIU Zhendong()   

  1. Department of Medical Oncology, The First Affiliated Hospital of Zhejiang University of Chinese Medicine, Zhejiang Hangzhou 310002, China
  • Received:2020-09-09 Online:2020-11-25 Published:2022-07-20
  • Contact: LIU Zhendong E-mail:liudong761@163.com

Abstract:

Objective To study on the expression of forkhead box D1 (FOXD1) in pancreatic cancer and the mechanism of invasion and metastasis of pancreatic cancer through FOXD1 via the extracellular signal-regulated kinase (ERK) pathway. Methods We searched the database of expression of FOXD1 in both pancreatic cancer and normal pancreatic tissue from the Cancer Genome Atlas and analyzed the difference in expression of FOXD1. Expression of FOXD1 mRNA in pancreatic tissue of 15 cases with pancreatic cancer was detected using polymerase chain reaction. Expression of FOXD1 in pancreatic cancer cell lines was analyzed using Western Blot. The effect of FOXD1 knockdown on the expression of proteins associated with epithelial mesenchymal transition(EMT) was investigated using Western Blot. The effect of FOXD1 knockdown on the proliferation and invasion of pancreatic cancer cell lines were tested by cell counting kit-8 assay and Transwell assay. Results FOXD1 was highly expressed in pancreatic cancer tissues and cell lines. Knockdown of FOXD1 attenuated the proliferation and invasion of pancreatic cancer cell lines and enhanced expression of EMT associa-ted proteins including epithelial cadherin and ERK while attenuated expression of neuronal cadherin and phosphorylated ERK. Conclusions FOXD1 would be the oncogene of pancreatic cancer by promoting invasion and metastasis of pancrea-tic cancer via ERK pathway.

Key words: Forkhead box D1, Pancreatic cancer, Epithelial-mesenchymal transition, Extracellular signal-regulated kinase pathway

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