Open AccessDownregulation of lncRNA‐HEIH curbs esophageal squamous cell carcinoma progression by modulating miR ‐4458/ PBX3
Author(s) -
Wang Dawei,
You Dong,
Pan Yinghua,
Liu Peiji
Publication year - 2020
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.13489
Subject(s) - downregulation and upregulation , cancer research , cell growth , western blot , gene silencing , cell , cell culture , esophageal squamous cell carcinoma , microrna , blot , medicine , biology , microbiology and biotechnology , carcinoma , pathology , gene , genetics
Background Long non‐coding RNAs (lncRNAs) have been found to play a specific part in the development of esophageal squamous cell carcinoma (ESCC), except for lncRNA HEIH. Here, we aimed to discover the molecular mechanisms of HEIH in ESCC. Methods We detected the expression level of HEIH and miR‐4458 in ESCC tissues and cells using qRT‐PCR assay. A dual luciferase reporter assay was used to check the relationship between HEIH, miR‐4458 or PBX3. Counting Clock Kit‐8 (CCK‐8) assay and transwell assay were used to detect ESCC cell proliferation and invasion capability. Western blot analysis was used to measure the protein expression level of PBX3. Results HEIH was confirmed to be upregulated in both ESCC tissues and cell lines. Inversely, there was a downregulation of miR‐4458 in ESCC tissues and cell lines. Functionally, we noticed that depletion of HEIH restrained ESCC cell viability, and invasion capability. Moreover, PBX silencing was found to restrain ESCC cell progression, while miR‐4458 or HEIH vector both could alleviate its suppressive effect. Conclusions The present study clarified that HEIH regulated ESCC progression by suppressing miR‐4458 and upregulating PBX3. Our findings suggested that HEIH could be a possible therapeutic target for ESCC treatment.