The transcriptomes in RGS10-depleted SKBR3 cells

RGS10 plays an important role in cell survival, polarization, adhesion,
chemotaxis, and differentiation in various cancers. However, the mechanism
underlying the function of RGS10 in breast cancer remains unclear. We
compared the gene expression differences between the RGS silencing group
and the wild group using RNA seq. The shRNA-RGS10 and shRNA negative
control (NC) are transfected in SKBR3 cells. We utilized a series of
functional experiments to verify the silencing of RGS10. The
transcriptomes in RGS10-depleted SKBR3 cells and shRNA-NC SKBR3 cells were
performed by second-generation high-throughput sequencing. This project
measured a total of 6 samples using the BGISEQ platform, with an average
output of 6.70G of data per sample. The average comparison rate of the
sample compared to the genome is 90.38%, and the average comparison rate
of the gene set is 70.96%; A total of 16606 genes were detected. By KEGG
enrichment analysis, upregulated KEGG pathways were found to be associated
with cytokine-cytokine receptor interactions and extracellular
matrix-receptor interactions. The biomarkers expression of EMT was
upregulated in RGS10-depleted SKBR3 cells compared to NC in Western
blotting. LCN2 and vimentin protein levels were higher and E-cadherin
protein levels were lower in RGS10-depleted SKBR3 cells compared to NC.
These findings show that RGS10 deficiency induces EMT by activating the
LCN2, supporting the potential of RGS10 as a prognostic biomarker in
breast cancer.