Fig 1: LINC00514 Knockdown suppresses the proliferation, invasion and expression of lipogenesis-related proteins in ESCC cells. (A) Reverse transcription-quantitative PCR assay of LINC00514 expression in various ESCC cell lines, including Eca109, KYSE150, KYSE30, KYSE450 and KYSE70 as well as in the normal esophageal epithelial Het-1A cell line. Data were compared using an ANOVA followed by a post hoc Dunnett's test. *P<0.05, **P<0.01, ***P<0.001 vs. Het-1A. (B) Three siRNAs specific for LINC00514 significantly downregulated the expression of LINC00514 in KYSE150 and KYSE30 cells. Data were compared using an ANOVA followed by a post hoc Dunnett's test. (C-E) LINC00514 siRNA2 suppressed the proliferation and invasion of KYSE150 and KYSE30 cells. (F) LINC00514 siRNA2 reduced the expression of lipogenesis-related proteins (SPHK1, FASN, ACACA and SCD1) in KYSE150 and KYSE30 cells. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. si-NC group. LINC00514, long intergenic nonprotein-coding RNA 00514; ESCC, esophageal squamous cell carcinoma; SPHK1, sphingosine kinase 1; FASN, fatty acid synthetase; ACACA, acetyl-CoA carboxylase α; SCD1, stearoyl-CoA desaturase 1; siRNA, small interfering RNA.
Fig 2: The correlation between CSC markers and proteins involved in lipid metabolism and their importance in the patient’s outcome. A The correlation heatmap with a hierarchical clustering of the levels of CSC markers and proteins involved in lipid metabolism. The magnitude of the correlation is shown by the colors with red representing a positive correlation and blue a negative correlation. B Kaplan-Meier curves representing the correlation between protein expression and recurrence. Low represents a low protein expression, high represents a high protein expression. CD cluster of differentiation, EpCAM epithelial cell adhesion molecule, ACLY ATP citrate lyase, SCD1 stearoyl-CoA desaturase-1. A p value lower than 0.05 was considered as a significant value
Fig 3: Validation of DEGs by qRT-PCR at the 4th day of differentiation in the FATP1 overexpression group infected with Ad-FATP1, Ad-NC (n = 3). (A) SLPI; (B) STC1; (C) SEMA6A; (D) TNFRSF19; (E) SLN; (F) PTGS2; (G) ADCYP1; (H) FADS2; (I) SCD. * p ≤ 0.05, ** p ≤ 0.01.
Fig 4: The summary of pathway analysis on differential metabolites between recurrence and non-recurrence, analyzed using MetaboAnalyst 4.0. A Metabolism pathway analysis from global metabolomics. B Metabolism pathway analysis from lipidomics. The color of the circle represents the p value, and the size of the circle represents the pathway impact. C The schematic diagram of metabolic pathways involved in CCA recurrence with red arrows indicating the most relevant pathway for recurrence. FAO fatty acid oxidation, CSC cancer stem cell, TG triacylglycerol, NEAAs non-essential amino acids, CD36 cluster of differentiation 36, ACLY ATP citrate lyase, SCD1 stearoyl-CoA desaturase-1
Fig 5: PPARα reversed the influence of MALAT1 on lipid accumulation induced by FFA in hepatocytes. (A) PPARα and CD36 expression were examined by qPCR. (B) TG level was detected by the TG assay kit. (C) Bodipy-labeled fatty acid uptake assay was used for assessment of fatty acid uptake. (D) Lipid accumulation was detected by Oil Red O staining. (E) SREBP1, ACC1, SCD1 and FASN levels were detected by qPCR. Data were presented as the mean ± SD. One-way analysis of variance was used among multiple groups. n = 3, *p < 0.05, **p < 0.01.
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