189P - LncRNA NKILA as a negative regulator of NFkB in ascites in ovarian cancer

Background

NF-κB-interacting LncRNA (NKILA) plays an inhibitory role in the NF-κB pathway, which is a key regulator of inflammatory cytokines. These mediators, freely floating in ascitic fluid (AF), reflecting the molecular genetic characteristics of tumor cells in ovarian cancer (OC), and associated with epigenetic switches of key pathways of carcinogenesis remain poorly understood. The aim of the work was to study the expression of LncRNA NKILA and marker cytokines of the NF-kB pathway in ascites of patients with OC.

Methods

The study included 22 patients with ascitic OC at stage III-IV according to FIGO. Isolation of circulating nucleic acid was performed from 2 ml of the cell-free fraction of ascites before treatment using SileksMagNaDirect magnetic particles (Sileks, Russia). lncRNA NKILA expression in AF was determined by qPCR (CFX-96, BioRad). Determination of cytokines VEGFA, IL-6, MCP-1 in AF was performed by ELISA. According to the effect of platinum-containing chemotherapy (CT), the patients were divided into groups: 1 - progression against the background of CT and early relapse; 2 - nonrelapsive. Statistical data processing was carried out using Statistica 13.0.

Results

The study included 22 patients with ascitic OC at stage III-IV according to FIGO. Isolation of circulating nucleic acid was performed from 2 ml of the cell-free fraction of ascites before treatment using SileksMagNaDirect magnetic particles (Sileks, Russia). lncRNA NKILA expression in AF was determined by qPCR (CFX-96, BioRad). Determination of cytokines VEGFA, IL-6, MCP-1 in AF was performed by ELISA. According to the effect of platinum-containing chemotherapy (CT), the patients were divided into groups: 1 - progression against the background of CT and early relapse; 2 – non-relapsive. Statistical data processing was carried out using Statistica 13.0.

Conclusions

Thus, the study of the lncRNA NKILA profile in tumor ascites in relation to inflammatory cytokines of the NF-kB signaling pathway requires further study in the context of understanding the signatures in the formation of chemoresistance in advanced OC.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.