Fig. 7

PLA2G16-mediated phospholipid metabolism and metabolite arachid-onic acid (AA) involve in LncROPM-driven BCSCs maintenance. A, B The altered lipid species in MCF7 BCSCs (A) with or without lncROPM, or MCF7 non-BCSCs (B) with or without ectopic lncROPM. Cer ceramide; HexCer hexosylceramide; GlcCer glucosylceramide; PA phosphatidic acid; PS phosphatidylserine; PI phosphatidylinositol; PE phosphatidylethanolamine; PC phosphatidylcholine; PG glycerophosphoglycerols; TG triglyceride; CL cardiolipin; SM sphingomyelin; FFA free fatty acid. C, D The top 5 changed FFAs in lncROPM-silenced MCF7 BCSCs group (C) or ectopic lncROPM-expressing MCF7 non-BCSCs group (D). E PLA2G16 in MCF-7 BCSCs were knocked down by shRNA or pre-treated with Giripladib (300 nM); the contents of AA were measured in these BCSCs and their control BCSCs. F, G The AA contents in MCF7 non-CSCs transfected with or without LV-ROPM (F), and in non-BCSCs and BCSCs derived from MCF7 and BT549 cells. H Western blotting to determine stemness-related proteins (SOX2, OCT4, and KLF4) in shCtrl group, shlncROPM-2 group treated with or without AA (100 µM) from BT549 BCSCs and MCF7 BCSCs for 7 days (a) or shCtrl group, shPLA2G16-2 group treated with or without AA (100 µM) from Hs578T BCSCs and MCF7 BCSCs for 7 days (b). Data are presented as the mean ± SD; *p < 0.05, **p < 0.01