Fig. 4: LPIAT1 is overexpressed in human lung cancer and predicts poor patient survival.
From: The ACSL3-LPIAT1 signaling drives prostaglandin synthesis in non-small cell lung cancer
a Relative LPIAT1 mRNA expression in healthy lungs (n = 59) or lung tumors from wild-type (n = 326) or mutant KRAS (n = 148) human lung adenocarcinomas (LUAD cohort). The box-plots span from the first to third quartile (depicting the median as a line in the middle), the whiskers extend to 1.5 x IQR (interquartile range). Outliers > 1.5 times the IQR are indicated with circles. b Relative LPIAT1 mRNA expression in LUAD cohort stratified by PTGES2-high (n = 258) versus PTGES2-low (n = 259) by median separation. Outliers >1.5 times the IQR are indicated with circles. c Immunoblot analysis of the indicated targets in primary human patient-derived lung adenocarcinoma samples. N normal lung, T lung tumor (lung adenocarcinomas). The mutational status of KRAS is indicated. d Relative LPIAT1 mRNA expression in squamous lung carcinoma (LUSC) and lung adenocarcinoma (LUAD) cohorts stratified by ACSL3-high (n = 508) versus ACSL3-low (n = 509) by median separation. Outliers > 1.5 times the IQR are indicated with circles. Kaplan–Meier analysis showing the percent survival of ACSL3-low versus ACSL3-high (e) or LPIAT1-low versus LPIAT1-high (f) in squamous lung carcinoma (LUSC) and lung adenocarcinoma (LUAD) cohorts. The number of patients is indicated. Statistical analyses were done using two-tailed unpaired Student’s t test, one-way ANOVA or log-rank (Mantel-cox) test. **p < 0.01, ****p < 0.0001.
