Upregulation of miR-194-5p or silencing of PRC1 enhances radiotherapy sensitivity in esophageal squamous carcinoma cells

• Published in: Heliyon Vol. 9; no. 12; p. e22282
• Main Authors: Wang, Yan, Yao, Ninghua, Sun, Jie
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01-12-2023; Elsevier
• Subjects: Esophageal squamous cell carcinoma; Invasion; Metastasis; miR-194-5p; PRC1; Radiotherapy sensitivity; Wnt/β-catenin; PRC1; Wnt/β-catenin; Esophageal squamous cell carcinoma; Radiotherapy sensitivity; miR-194-5p; Metastasis; Invasion
• ISSN: 2405-8440; 2405-8440
• DOI: 10.1016/j.heliyon.2023.e22282

To investigate the possible molecular mechanism of miR-194-5p/PRC1/Wnt/β-catenin signaling axis that regulates the invasive metastatic ability and radiotherapy sensitivity of esophageal squamous cell carcinoma (ESCC) cells.
ESCC-related differentially expressed miRNAs were identified by microarray analysis, followed by the identification of a putative target. The targeting relationship between miR-194-5p and PRC1 was assayed. A series of mimic and shRNA were transfected into ESCC cells to find out the mechanism of miR-194-5p in ESCC by regulating PRC1 through Wnt/β-catenin signaling pathway and their effect on cell proliferation, migration, invasion, and radiosensitivity as well as xenograft tumor growth and metastasis in nude mice.
We demonstrated low miR-194-5p expression and high PRC1 expression in ESCC tissues and cells. PRC1 was confirmed as a putative target for miR-194-5p. High miR-194-5p or silenced PRC1 enhanced ESCC cell radiosensitivity but reduced proliferation, invasion, and migration via PRC1 through modulation of the Wnt/β-catenin signaling pathway. Animal experiments also validated that overexpression of miR-194-5p suppressed tumorigenesis and in vivo metastasis in nude mice.
Conclusion: miR-194-5p can inhibit the Wnt/β-catenin signaling pathway through down-regulation of the PRC1 gene, thereby enhancing the sensitivity of ESCC cells to radiotherapy and attenuating the invasion and metastasis ability of ESCC cells.