Lnc-LFAR1 affects intrahepatic cholangiocarcinoma proliferation, invasion, and EMT by regulating the TGFβ/Smad signaling pathway.

Intrahepatic cholangiocarcinoma (ICC) has had an increasing incidence in recent years. It exhibits high recurrence and metastasis rates, so it is a global health problem. LncRNAs have long been thought to have a role in regulating tumorigenesis and tumor progression and in playing a carcinogenic or tumor suppressor role in malignant cells. Lnc-LFAR1 is enriched in liver tissue, but its role and mechanism in ICC have not been elucidated. ICC cell line QBC939 cells were randomly divided into 3 groups, including a control group, an lnc-LFAR1 overexpression group, and an lnc-LFAR1 siRNA group, the cells of which were transfected with pcDNA3.1-LFAR1 plasmid and lnc-LFAR1 siRNA, respectively. Real-time PCR was used to quantify lnc-LFAR1 expression. A tetrazolium salt (MTT) colorimetric assay was adopted to assess cell viability. A cell scratch assay was selected to assess cell migration. A transwell chamber assay was used to test cell invasion. E-cadherin and vimentin expressions were detected using Western blot. The TGFβ/Smad signaling pathway was measured using real-time PCR. The transfection of pcDNA3.1-LFAR1 significantly increased the expression of lnc-LFAR1, promoted cell proliferation, facilitated cell migration and invasion, reduced E-cadherin levels, enhanced vimentin expression, upregulated TGF-β1 and Smad2 and Smad4 expressions (P < 0.05). Lnc-LFAR1 siRNA transfection clearly downregulated lnc-LFAR1 expression, inhibited cell proliferation, suppressed cell migration and invasion, increased E-cadherin expression, and decreased vimentin, TGF-β1, Smad2, and Smad4 levels (P < 0.05). Targeting lnc-LFAR1 can inhibit cell proliferation, migration, invasion, and EMT by regulating the TGFβ/Smad pathway to affect the occurrence and development of cholangiocarcinoma.