RBPMS expression

There also existed a targeting relationship and negative interplay between PLCL1 and miR-19a-3p. In short, RBPMS-AS1 sponges miR-19a-3p and represses the growth and EMT of CC cells via enhancing PLCL1-mediated pyroptosis.

MiR-19a-3p targeted PTEN and miR-19a-3p mimic reversed the effect of overexpressed RBPMS-AS1 on PTEN and phosphorylation of AKT in LC cells. Overexpressed RBPMS-AS1 sponged miR-19a-3p to increase cell radiosensitivity in LC via regulating PTEN/AKT axis.

These studies suggest that increased levels of RBPMSA and RBPMSC reduce cell proliferation in ovarian cancer cells. However, only RBPMSA expression levels were associated with the sensitivity of ovarian cancer cells to cisplatin treatment.

The combination of AKT inhibitor MK2206 and gefitinib had a synergistic effect on OC cells with high level of RBPMS. In conclusion, through the direct inhibition of HER2/AKT/mTOR/P70S6K pathway, RBPMS may be a potential therapeutic target for improving gefitinib sensitivity in OC.

However, only the isoform A contributed to the cisplatin sensitivity of ovarian cancer cells. Future efforts on this project will be focused on determining the RBPMS isoform that represses AP-1 (c-Fos and c-Jun) dependent gene regulation in cisplatin sensitive ovarian cancer cells.

We also focus on the correlation analysis between EMT-related genes and RBPMS2/ESRP1. Finally, we analysed the correlation between RBPMS2 expression and chemotherapeutic drugs which may assist in GC therapy and demonstrated that RBPMS2 expression was associated with tumour mutation burden (TMB) and Microsatellite Instability (MSI), as well as immune infiltration level in GC.