TY - JOUR AB - The aim of the present study was to investigate the functional role of Frizzled-7 (FZD7) in the apoptosis of hepatoma cells. HepG2 and Huh‑7 hepatocellular carcinoma (HCC) cell lines with FZD7 expression were selected for use in the present study. The small hairpin RNA (shRNA) eukaryotic expression vector specific to FZD7 was constructed using gene recombination, and was then transfected into HepG2 and Huh‑7 hepatoma cell lines using Lipofectamine 2000 to assess whether the downregulation of FZD7 could affect the proliferative ability of these cells. The results demonstrated that the downregulation of FZD7 expression significantly inhibited the proliferative ability of both cell types through the induction of cell apoptosis, as evidenced using Cell Counting kit‑8 assays and flow cytometry. Furthermore, the western blotting results demonstrated that silencing of FZD7 increased the activities of caspase‑3 and caspase‑9. These increases were also associated with the downregulation of the inhibitor of the apoptosis protein family. Additionally, it was revealed that silencing of FZD7 expression caused the downregulation of apoptosis regulator Bcl‑2 and Bcl‑XL in HepG2, and Huh‑7 cells, as determined through western blot analysis and reverse transcription‑quantitative polymerase chain reaction. In the following work, ELISA and western blot analysis revealed that the knockdown of FZD7 inhibited the expression and activities of nuclear factor‑κB (NF‑κB) p65. Furthermore, it was demonstrated that the expression levels of phosphylated‑Smad2/3 were markedly upregulated in sh‑FZD7‑transfected HepG2 and Huh‑7 cells. Then, shRNA eukaryotic expression vector specific to transforming growth factor (TGF)‑β receptor II was transfected into both cell lines to investigate the association between the TGF‑β/Smad signaling pathway and NF‑κB p65. Notably, when the TGF‑β/Smad signaling pathway was inhibited, no significant differences in the cell apoptosis rate and NF‑κB expression levels were identified in HCC cells. Overall, the results of the present study suggest that the shRNA‑mediated knockdown of FZD7 induces apoptosis of hepatoma cell lines through the inhibition of NF‑κB. In addition, the TGF‑β/Smad signaling pathway appeared to partially participate in the underlying molecular mechanism of FZD7 in HCC. AD - Department of Interventional Radiology, The No. 1 Hospital of Xuzhou, Xuzhou, Jiangsu 221002, P.R. China State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China Department of Interventional Radiology, Affiliated Hospital of Xuzhou Medical College, Xuzhou, Jiangsu 221002, P.R. China Jiangsu Key Laboratory of Biological Cancer Therapy, Xuzhou Medical College, Xuzhou, Jiangsu 221002, P.R. China AU - Xue,Yuyang AU - Chen,Cong AU - Xu,Wei AU - Xu,Hao AU - Zheng,Junnian AU - Gu,Yuming DA - 2018/05/01 DO - 10.3892/ol.2018.8292 EP - 7701 IS - 5 JO - Oncol Lett KW - frizzled‑7 hepatocellular carcinoma apoptosis nuclear factor‑κB transforming growth factor‑β/Smad PY - 2018 SN - 1792-1074 1792-1082 SP - 7693 ST - Downregulation of Frizzled-7 induces the apoptosis of hepatocellular carcinoma cells through inhibition of NF-κB T2 - Oncology Letters TI - Downregulation of Frizzled-7 induces the apoptosis of hepatocellular carcinoma cells through inhibition of NF-κB UR - https://doi.org/10.3892/ol.2018.8292 VL - 15 ER -