FAT1 and PTPN14 Regulate the Malignant Progression and Chemotherapy Resistance of Esophageal Cancer through the Hippo Signaling Pathway

Anal Cell Pathol (Amst). 2021 Oct 19:2021:9290372. doi: 10.1155/2021/9290372. eCollection 2021.

Abstract

Background: Esophageal cancer (EC) is a common malignant tumor, which brings heavy economic burden to patients and society. Therefore, it is important to understand the molecular mechanism of recurrence, metastasis, and drug resistance of esophageal cancer.

Methods: Human esophageal cancer cell line TE13 (poorly differentiated squamous cell carcinoma) and normal human esophageal epithelial cell line het-1a were selected for aseptic culture. At the same time, 6 bottles of TE13 cell line were inoculated in logarithmic phase. Cell apoptosis was analyzed by flow cytometry (FCM). Cell clone formation assay was used to analyze the proliferation. Fibronectin-coated dishes were used to detect the characteristics of cell adhesion to extracellular matrix. The Transwell method was used to detect the cell invasion ability. Western blot was used to analyze the expression of Yap1, PTPN14, FAT1, and Myc.

Results: Results showed that FAT1 and PTPN14 were downregulated, while Yap1 was upregulated in esophageal cancer tissues. FAT1 inhibited the proliferation, adhesion, and invasion of human esophageal cancer cell lines, which might be associated with the upregulation of PTPN14 and the inhibition of Yap1 and Myc.

Conclusion: The results suggested that PTPN14 and FAT1 could regulate malignant progression and chemotherapy resistance of esophageal cancer based on the Hippo signaling pathway.

MeSH terms

  • Cadherins / metabolism*
  • Disease Progression
  • Drug Resistance, Neoplasm / physiology*
  • Esophageal Neoplasms / metabolism*
  • Esophageal Neoplasms / pathology
  • Hippo Signaling Pathway / physiology*
  • Humans
  • Protein Tyrosine Phosphatases, Non-Receptor / metabolism*

Substances

  • Cadherins
  • FAT1 protein, human
  • PTPN14 protein, human
  • Protein Tyrosine Phosphatases, Non-Receptor