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LncRNA LINC00467 acted as an oncogene in esophageal squamous cell carcinoma by accelerating cell proliferation and preventing cell apoptosis via the miR‐485‐5p / DPAGT1 axis
Author(s) -
Liu Zhenghua,
Yang Shize,
Chen Xitao,
Dong Siyuan,
Zhou Siyu,
Xu Shun
Publication year - 2021
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.15201
Subject(s) - cell growth , cancer research , apoptosis , oncogene , cell , gene knockdown , medicine , downregulation and upregulation , biology , cell cycle , gene , biochemistry , genetics
Background and Aim Esophageal carcinoma has been regarded as one of the top 10 common malignancies globally. Esophageal squamous cell carcinoma (ESCC) is an important subtype of esophageal carcinoma with approximately 20% survival rate. Long noncoding RNAs were documented to regulate the occurrence or progression of several tumors. However, neither the biological role nor the molecular mechanism of LINC00467 has been explored. This research is aimed to investigating the regulatory mechanism of LINC00467 in ESCC. Methods In this study, a series of experiments including reverse transcription–quantitative polymerase chain reaction, Cell Counting Kit‐8, luciferase reporter, western blot, and RNA immunoprecipitation were designed and conducted to explore the potential function and mechanism of LINC00467 in ESCC. Results According to experimental results, we found out upregulated LINC00467 improved cell proliferation, but hindered cell apoptosis. In mechanism, miR‐485‐5p was predicted, screened out, and validated to combine with LINC00467 , which displayed lower expression in ESCC. Additionally, miR‐485‐5p negatively regulated and directly targeted DPAGT1 . Rescue assays suggested that DPAGT1 amplification was able to recover the influence of LINC00467 deficiency on cell proliferation and apoptosis. Furthermore, knockdown of LINC00467 suppressed tumor growth in vivo. Conclusion We proved that LINC00467 acted as an oncogene in ESCC by accelerating cell proliferation and preventing cell apoptosis via miR‐485‐5p / DPAGT1 axis. This may provide a potential diagnostic marker for ESCC treatment.