Research Paper Volume 13, Issue 4 pp 4986—4998

Loss of FBP1 promotes proliferation, migration, and invasion by regulating fatty acid metabolism in esophageal squamous cell carcinoma

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Figure 4. FBP1 was interacted with miR-18b-5p in Eca109 cells. (A) Cell lysates prepared from Eca109 cells were incubated with antibodies against IgG, Glut4, FBP1, PFK, PKM2, c-Myc, P53, AMPK, FABP4, FASN, Ccnd1, Cdk4, CD36, Cpt1a, Prkaa1, Adipoq, Cfd and Retn. The precipitated products were subjected to real-time PCR with primers amplifying miR-18b mRNA. Error bars, SD (n = 4). **p < 0.01, ***p < 0.001. (B) The prediction of miR-18b-5p and 3’UTR of FBP1 targeting site. (C) miR-18b-5p mimic directly targeted the wt of FBP1 in Eca109 cells. (D) The pulled down FBP1 in the Bio-miR-18b-5p transfected cells. (E) Enrichment of FBP1 transcripts in Bio-miR-18b-5p pull-down mRNA in Eca109 cells. (F) The FBP1 expression was determined following treatment with miR-18b-5p mimic or inhibitor. Wt, wild-type reporter plasmid containing FBP1 3’UTR; mut, mutations reporter plasmid in the same regions. Mimic control, the miR-18b-5p mimic negative control group. Bio-NC, biotin-labeled negative control. Bio-miR-18b-5p, biotin-labeled miR-18b-5p. Inhibitor control, the miR-18b-5p inhibitor negative control group. *p< 0.05, **p< 0.01 VS respective control.