Fig 1: High expression of LPL was associated with poor prognosis in PTC. (A) LPL expression in tissue samples was measured using western blotting (WB). Representative WB diagrams of LPL expression are shown in the top panel. The quantification data are shown in the lower panel, **p < 0.01. The error bar indicates s.d., two-tailed unpaired t-test. P indicates para-tumour, T indicates tumour. (B) LPL expression and localisation were evaluated using tissue microarray. The left panel shows immunohistochemical staining for LPL (brown) with Mayer’s haematoxylin counterstain. Scale bar 100µm. Statistical data of LPL protein expression in 58 paired samples are shown in the right panel. ****p < 0.0001. Error bar indicates s.d., two-tailed unpaired t-test. (C) Data of LPL mRNA levels were obtained from publically available dataset (GSE104006). **p < 0.01. The error bar indicates s.d., student t-test. (D) Statistical analysis of LPL expression in tissue microarray. Chi-square test was used to analyse significant differences, ****p < 0.0001. (E) Correlation between LPL expression and stages of thyroid cancer. The graph in the left panel shows that LPL expression was positively correlated with the T stage in PTC. The graph in the middle panel shows that LPL expression was positively correlated with the N stage in PTC. The graph in the right panel shows that LPL expression was positively correlated with the TNM stage in PTC. ****p < 0.0001, **p < 0.01; ns indicates: not statistically significant. All error bars indicate s.d., two-tailed unpaired t-test.
Fig 2: Effects of miR-483 on adipogenic differentiation of hADSCs. (A, B) The efficiency of miR-483-5p and miR-483-3p inhibition was assayed by RT-qPCR. (C) The effect of inhibition of miR-483-3p and miR-483-5p on adipogenic differentiation of hADSCs was evaluated on day 14 using Oil Red O staining (10×; scale: 50µm). (D–F) RT-qPCR and western blot analysis of LPL and PPAR? expression levels. I-CT: negative control inhibitor; 483-5p-I: inhibitor of miR-483-5p; 483-3p-I: inhibitor of miR-483-3p.
Fig 3: Activated lipid metabolism in thyroid carcinoma. (A) Overexpression of LPL, FATP2 and CPT1A in BHP10-3 cells were confirmed by western blot. (B) Cell migration was examined in BHP10-3 cells with LPL, FATP2 and CPT1A overexpression. ***p < 0.001, ****p < 0.0001. All error bars indicate s.d., two-tailed unpaired t-test. (C) As shown, long-chain fatty acids (LCFAs) are released from triglycerides (TGs) by lipoprotein lipid (LPL) and transported to cells by fatty acid transport protein 2 (FATP2). Carnitine palmitoyltransferase 1A (CPT1A) controls the utilisation of LCFA for energy supply. Furthermore, LCFAs can be used for cell construction and signal transduction. Red indicates up-regulation and blue indicates down-regulation. TG, triglyceride; FABP, fatty acid binding protein; ACS, Acyl-coenzyme A synthetase; CPT2, Carnitine palmitoyltransferase 2; MCAT, mitochondria carnitine acylcarnitine translocase.
Supplier Page from Abcam for Anti-Lipoprotein lipase antibody [EPR1555(2)]