Introduction/Background Previously, we identified lipolysis-stimulated lipoprotein receptor (LSR) as a poor prognostic factor of epithelial ovarian cancer (EOC), and we demonstrated anti-cancer effect of our newly developed anti-LSR monoclonal antibody (mAb) against LSR-positive EOC in vitroand in vivo. We also demonstrated that LSR took up VLDL and promoted cell proliferation, however, lipid metabolic pathway via LSR is still unclear. Thus, we aimed to reveal the function of LSR in lipid metabolism in EOC cells.

Methodology We administrated fatty acid to LSR-positive EOC cells and investigated the activation of beta-oxidation, ATP production, cell proliferation and cell migration via LSR. We also investigated anti-cancereffect of our anti-LSR mAb against lipid metabolism via LSR.

Results We administrated fatty acids (Palmitic acid (PA), Myristic acid (MA), Arachidonic acid (AA), Oleic acid (OA) and Elaidic acid (EA)) to LSR-positive and LSR-knockdown EOC cell lines, respectively. OA and EA promoted cell proliferation of LSR-positive cells, however, PA, MA and AA did not. Although OA promoted cell proliferation of LSR-positive cells, EA did not, meaning that EA bind to LSR specifically and promoted cell proliferation via LSR. In LSR-positive EOC cells, EA administration increased intracellular lipid accumulation. Moreover, EA promoted ATP production (p<0.05), suggesting that beta-oxidation, TCA cycle and electron transport system were activated by Elaidic acid in LSR-positive EOC cells. Furthermore, in LSR-positive EOC cells, Elaidic acid administration promoted cell migration (p<0.05). Finally, our anti-LSR mAb inhibited these processes (p<0.05).

Conclusion Elaidic acid uptake via LSR in lipid metabolic pathway contributed to cell viability and cancer spread, and anti-LSR mAb inhibited these processesin LSR-positive EOC cells. Anti-LSR mAb might be a therapeutic agent against human EOC.

Disclosure Nothing to disclose.