Fig. 7: NanoFEN inhibits cellular metabolism in lung cancer spheroid cells (LCSCs) and CRC spheroid cells (CSCs).

a Schematic representation of RPPA results of proliferative and biosynthetic pathways repressed (grey) in LCSCs treated with NanoFEN. b Immunoblot analysis of proteins involved in metabolic process on LCSC6 (left panel) and CSC7 (right panel) untreated and treated with NanoFEN at IC50 dose (4.9 and 0.2 μM, respectively) for 48 h. c Graphs represent NanoFEN effects on lipid metabolism by liquid chromatography-mass spectrometry (LC-MS) on LCSC6 (left panel) and CSC7 (right panel). Values represents the fold over control of treated cells with NanoFEN (4.9 and 0.2 μM, respectively) for 24 h. d Sphinganine peak intensity in LCSC6 (left panel) and CSC7 (right panel) treated with NanoFEN (4.9 and 0.2 μM, respectively) for 24 h. e Cell viability of LCSC6 (left panel) and CSC7 (right panel) treated with Myriocin 1 μM plus NanoFEN (4.9 and 0.2 μM, respectively) for 48 h. Values represent mean ± SD of three independent experiments. *P < 0.05, from two-tailed t-test. f Cell viability of LCSC6 (left panel) and CSC7 (right panel) treated with glucosylceramide synthase inhibitor PPMP 10 μM plus NanoFEN (4.9 and 0.2 μM, respectively) for 48 h. Values represent mean ± SD of three independent experiments. *P < 0.05, from two-tailed t-test. g Cell viability of LCSC6 (left panel) and CSC7 (right panel) treated with dihydroceramide desaturase inhibitor (GT11) 0.5 μM plus sphinganine (SA) 2 μM plus mTOR pathway inhibitor Rapamycin 10 nM for 48 h. Values represent mean ± SD of three independent experiments. *P < 0.05; ***P < 0.001, from two-tailed t-test. h Immunoblot analysis of mTOR pathway components mTOR, phospho-mTOR, S6RP and phospho-S6RP on LCSC6 (left panel) and CSC7 (right panel) treated as in (g)