miR‐132‐3p promotes heat stimulation‐induced esophageal squamous cell carcinoma tumorigenesis by targeting KCNK2

Author:

Wang Jing123,Li Jiaqiong124,Cheng Dan12,Zhang Keke12,Liu Wenting12,Xue Qianqian15,Du Ruijuan12,Zhou Liting12,Yeung Yiu To2,Bai Ruihua6,Huang Hui1,Cui Jie1,Xiang Pu2,Zhi Yafei2,Liu Kangdong1278,Li Xiang1278ORCID,Dong Zigang1278

Affiliation:

1. Department of Pathophysiology, School of Basic Medical Sciences Zhengzhou University Zhengzhou Henan China

2. China‐US (Henan) Hormel Cancer Institute Zhengzhou Henan China

3. Armed Police Hospital of Henan Zhengzhou Henan China

4. Department of Pathology The New Area People's Hospital of Luoyang Luoyang Henan China

5. Department of Public Health Nanshi Hospital of Nanyang Nanyang Henan China

6. The Affiliated Cancer Hospital Zhengzhou University Zhengzhou Henan China

7. Collaborative Innovation Center of Henan Province for Cancer Chemoprevention Zhengzhou Henan China

8. State Key Laboratory of Esophageal Cancer Prevention and Treatment Zhengzhou University Zhengzhou Henan China

Abstract

AbstractEpidemiological evidence supports that consumption of high‐temperature food and beverages is an important risk factor for esophageal squamous cell carcinoma (ESCC); however, the underlying mechanism still remains unclear. Here, we established a series of animal models and found that drinking 65°C water can promote esophageal tumor progression from preneoplastic lesions to ESCC. RNA sequencing data showed that miR‐132‐3p was highly expressed in the heat stimulation group compared with controls. Further study verified that miR‐132‐3p were upregulated in human premalignant lesion tissues of the esophagus, ESCC tissues, and cells. Overexpression of miR‐132‐3p could promote ESCC cell proliferation and colony formation, whereas knockdown of miR‐132‐3p could inhibit ESCC progression in vitro and in vivo. Importantly, dual‐luciferase reporter assays showed that miR‐132‐3p could bind with the 3′‐untranslated region of KCNK2 and inhibit KCNK2 gene expression. Knockdown or overexpression of KCNK2 could promote or suppress ESCC progression in vitro. These data suggest that heat stimulation can promote ESCC progression and miR‐132‐3p mediated this process by directly targeting KCNK2.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Cancer Research,Molecular Biology

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