Mechanism of circHMGCS1/miR-335-5p/ITGB2 in regulating the proliferation,migration and invasion of breast cancer MDA-MB-231 cells
LI Fei
LIU Jia-wei
LU Cheng-fei
ZHANG Zhi-hui
Abstract:Objective To investigate the effect of circular RNA HMGCS1(circHMGCS1)/microRNA-335-5p(miR-335-5p)/integrin β2(ITGB2)molecular axis on the proliferation,migration and invasion of breast cancer(BC)MDA-MB-231 cells and its possible mechanism.Methods A total of 47 BC tissues and adjacent tissues(>5 cm to the lesions)were collected in our hospital from May 2020 to November 2020.qRT-PCR and Western blot were used to detect the expression of circHMGCS1,miR-335-5p,and ITGB2 protein.sh-NC,sh-circHMGCS1,miR-NC,and miR-335-5p mimics were transfected into MDA-MB-231 cells,respectively.Cell viability,scratch healing rate,and number of invasive cells were detected respectively.The dual luciferase reporter assay was used to detect the targeting relationship between circHMGCS1 and miR-335-5p,miR-335-5p and ITGB2.Results Compared with the adjacent tissue,the protein expression of circHMGCS1 and ITGB2 in BC tissue was increased(P<0.05),while the expression of miR-335-5p was decreased(P<0.05).Compared with transfection of sh-NC or miR-NC,after transfection of sh-circHMGCS1 or miR-335-5p mimics,cell viability,wound healing rate was decreased(P<0.05),the number of invasive cells was decreased(P<0.05).circHMGCS1 targeted to regulate the expression of miR-335-5p,and miR-335-5p targeted to regulate the expression of ITGB2.Conclusion Interfering with the expression of circHMGCS1 could up-regulate the expression of miR-335-5p and down-regulate the expression of ITGB2,thereby inhibiting the proliferation,migration and invasion of BC cells.
Keywords:Breast cancerCircular RNA HMGCS1MicroRNA-335-5pIntegrin β2
Publication Date:2023-08-28
Online Publishing Date:2025-08-15(First online date of this platform, not the publication date of the document)
Pages:6( 739-743,793 )
Chinese Journal of Diagnostic Pathology

Chinese Journal of Diagnostic Pathology

ISTIC
ISSN:1007-8096
Year, Vol.(Issue):2023,30(8)