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

Yingzhi Lu,Ling Zhou,Yan Wu,Yan Shao,Jianguo Zhang,Yunyun Yang,Zhaoming Ma,Zhenxin Wang,Lubna H Tahtamouni

doi:10.1155/2021/9290372

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.

Highlights

Esophageal cancer (EC) is a common malignant tumor of the digestive tract, which brings heavy economic burden to patients and society [1]
Knockdown of FAT1 significantly downregulated the protein level of Protein tyrosine phosphatase nonreceptor type 14 (PTPN14) and increased the protein levels of Yap1 and Myc (Figure 7). These data showed that FAT1 inhibited the cell proliferation, adhesion, and invasion of human esophageal cancer, which might be associated with the upregulation of PTPN14 and inhibition of Yap1 and Myc
We examined the expression levels of Yap1, PTPN14, and FAT1 in human esophageal cancer cell lines and tissues

Summary

Background

Esophageal cancer (EC) is a common malignant tumor, which brings heavy economic burden to patients and society. It is important to understand the molecular mechanism of recurrence, metastasis, and drug resistance of esophageal cancer. 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 Yap, PTPN14, FAT1, and Myc. Results. Results showed that FAT1 and PTPN14 were downregulated, while Yap 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 Yap 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

Introduction

Material and Methods

Result

Discussion