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Long non-coding RNA KCNQ1 overlapping transcript 1 promotes the progression of esophageal squamous cell carcinoma by adsorbing microRNA-133b
Xu, Haitao; Miao, Jing; Liu, Shuai; Liu, Hongjian; Zhang, Lianguo; Zhang, Qingguang.
Affiliation
  • Xu, Haitao; Binzhou Medical University Hospital. Department of Thoracic Surgery. Binzhou. CN
  • Miao, Jing; Binzhou Peoples Hospital. Department of Pediatrics. Binzhou. CN
  • Liu, Shuai; Binzhou Medical University Hospital. Department of Thoracic Surgery. Binzhou. CN
  • Liu, Hongjian; Binzhou Medical University Hospital. Department of Thoracic Surgery. Binzhou. CN
  • Zhang, Lianguo; Binzhou Medical University Hospital. Department of Thoracic Surgery. Binzhou. CN
  • Zhang, Qingguang; Binzhou Medical University Hospital. Department of Thoracic Surgery. Binzhou. CN
Clinics ; Clinics;76: e2175, 2021. tab, graf
Article de En | LILACS | ID: biblio-1249578
Bibliothèque responsable: BR1.1
ABSTRACT

OBJECTIVE:

The long non-coding RNA (lncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) exerts vital regulatory functions in diverse tumors. However, the biological function of KCNQ1OT1 in esophageal squamous cell carcinoma (ESCC) remains unclear.

METHODS:

KCNQ1OT1 expression was detected in ESCC tissues using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, migration, and invasion were detected by the CCK-8 assay, EdU assay, flow cytometry analysis, and Transwell experiments, respectively. Bioinformatics analysis, luciferase reporter experiments, and RNA immunoprecipitation assays were used to predict and validate the regulatory relationships between KCNQ1OT1, microRNA-133b (miR-133b) and epidermal growth factor receptor (EGFR).

RESULTS:

KCNQ1OT1 expression was remarkably upregulated in ESCC tissues and cell lines. Overexpression of KCNQ1OT1 markedly promoted ESCC cell proliferation, migration, and invasion and enhanced the expression of N-cadherin, MMP-2, and MMP-9, but inhibited apoptosis and E-cadherin expression in ESCC cell lines; KCNQ1OT1 knockdown exerted the opposite effects. KCNQ1OT1 could directly bind to miR-133b and suppress its expression, and miR-133b reversed the effects of KCNQ1OT1 overexpression in ESCC cells. MiR-133b reduced the expression of epidermal growth factor receptor (EGFR); further, KCNQ1OT1 activated the phosphatidylinositol 3-kinase/AKT serine/threonine kinase 1 (PI3K/AKT) signaling pathway by repressing miR-133b repression and indirectly upregulating EGFR. KCNQ1OT1 expression was positively correlated with EGFR mRNA expression and negatively correlated with miR-133b expression.

CONCLUSION:

KCNQ1OT1 facilitates ESCC progression by sponging miR-133b and activating the EGFR/PI3K/AKT pathway.
Sujet(s)
Mots clés

Texte intégral: 1 Indice: LILACS Sujet Principal: Tumeurs de l'oesophage / MicroARN / ARN long non codant / Carcinome épidermoïde de l'oesophage Type d'étude: Prognostic_studies Limites du sujet: Humans langue: En Texte intégral: Clinics Thème du journal: MEDICINA Année: 2021 Type: Article

Texte intégral: 1 Indice: LILACS Sujet Principal: Tumeurs de l'oesophage / MicroARN / ARN long non codant / Carcinome épidermoïde de l'oesophage Type d'étude: Prognostic_studies Limites du sujet: Humans langue: En Texte intégral: Clinics Thème du journal: MEDICINA Année: 2021 Type: Article