Circ_0001955 plays a carcinogenic role in breast cancer via positively regulating GLUT1 via decoying miR‐1299

Autor: Hong Cheng, Sijie Kuang, Lingzhen Tan, Shengrong Sun
Jazyk: angličtina
Rok vydání: 2022
Předmět:
Zdroj: Thoracic Cancer, Vol 13, Iss 7, Pp 913-924 (2022)
Druh dokumentu: article
ISSN: 1759-7714
1759-7706
DOI: 10.1111/1759-7714.14310
Popis: Abstract Background Breast cancer is widespread in females. The role of circular RNA (circRNA) in breast cancer has aroused much attention. However, the function of several circRNAs remain unclear. The aim of our study was to determine the role of circ_0001955 in breast cancer. Methods Quantitative real‐time PCR (qPCR) and western blot was employed for expression analysis of circ_0001955, miR‐1299 and glucose transporter 1 (GLUT1). Cell functions including proliferation, apoptosis, migration, invasion and angiogenesis, were assessed using EdU, flow cytometry, transwell and tube formation assays. Glycolysis metabolism was assessed according to glucose consumption, lactate production and ATP content. Dual‐luciferase reporter assay and RIP assay were utilized to validate the binding between miR‐1299 and circ_0001955 or GLUT1. The effects of circ_0001955 in vivo were observed by animal study. Results Upregulation of circ_0001955 was detected in breast cancer. Knockdown of circ_0001955 inhibited breast cancer cell proliferation, migration, invasion, angiogenesis and glycolysis. MiR‐1299 was a target of circ_0001955, and its repression reversed the effects of circ_0001955 knockdown. Moreover, circ_0001955 targeted miR‐1299 to positively regulate GLUT1 expression. GLUT1 overexpression reversed the effects of miR‐1299 enrichment. GLUT1 knockdown was verified to block tumor growth in vivo. Conclusions Circ_0001955 was found to promote breast cancer malignant development via targeting of the miR‐1299/GLUT1 pathway, which contributes to our understanding of the pathogenesis of breast cancer.
Databáze: Directory of Open Access Journals
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje