Fig. 7: The hnRNPL-PIK3CB-AKT axis promotes ovarian cancer progression.

a Ovarian cancer cells were transfected with hnRNPL for 48 h. Then, cells were treated with TGX221 (5 μM) or PI-103 (5 μM), or DMSO as the negative control for 24 h for western blot. b CCK-8 assay detecting the growth of ovarian cancer cells described in (a). c Glucose content and lactate production were monitored in ovarian cancer cells described in (a). d hnRNPL was knocked down in ovarian cancer cells and then treatment with SC79 (5 μM) or DMSO as the negative control for 24 h was performed for western blot. e CCK-8 assay detecting the growth of ovarian cancer cells described in (d). f Glucose content and lactate production were monitored in ovarian cancer cells described in (d). g ATP content was measured in ovarian cancer cells described in (a) and (d). h, i ECAR levels were determined in ovarian cancer cells described in (a) by the Seahorse assays. j, k ECAR levels were determined in ovarian cancer cells described in (d) by the Seahorse assays. l Immunohistochemical staining assays detecting the protein expression of hnRNPL in ovarian cancer and ovarian epithelium tissues. Scale bar, 200 μm. m The overall survival and progression-free survival of patients with ovarian cancer with different hnRNPL levels according to the TCGA ovarian cancer database. n The overall survival, disease-free survival, and disease-specific survival of patients with ovarian cancer with hnRNPL gene alternations according to the TCGA ovarian cancer database. Data are shown as means ± S.D. p value was calculated by one-way ANOVA test with multiple comparisons (b, c, e–g, i, k) and two-sided Log-rank (Mantel-Cox) test (m, n). Data are representative of at least three independent experiments (a–k). Source data are provided as a Source Data file.