Effects of cullin 4B on the proliferation and invasion of human gastric cancer cells.

The major aim of the present study was to explore the effects of cullin 4B (CUL4B) on the proliferation and invasion of human gastric cancer cells. Gastric tumor tissues and paired adjacent non‑tumor tissues were obtained from 21 gastric cancer patients, and gastric cancer cell lines (AGS, MGC‑803, KATO‑III, MKN‑45, SGC‑7901, BGC‑823 and MKN‑74) were cultured. BGC‑823 cells were transfected with CUL4B small interfering (si)RNA or control siRNA. Reverse transcription‑quantitative polymerase chain reaction analysis was performed to detect the mRNA expression of CUL4B. Western blot analysis was performed to measure the protein levels of Wnt, β‑catenin, glutathione synthase kinase (GSK)‑3β, caspase‑3 and cyclin E. MTT and Transwell assays were performed to examine cell proliferation and invasion following CUL4B knockdown. In addition, the effect of CUL4B knockdown on the cell cycle and apoptosis of BGC‑823 cells was evaluated by flow cytometric analysis. The results indicated that compared with the adjacent non‑tumor tissues and a normal gastric epithelial cell line, gastric cancer tissues and cell lines exhibited significantly higher expression of CUL4B. Knockdown of CUL4B in gastric cancer cells suppressed cell proliferation, caused G1 arrest and inhibited cell invasion. Silencing of CUL4B also resulted in decreased Wnt and β‑catenin expression, but increased expression of GSK‑3β, caspase‑3 and cyclin E. These results indirectly demonstrate that CUL4B enhances the proliferation and invasion abilities of gastric cancer cells by upregulating the constituent factors Wnt and β‑catenin, as well as by negatively regulating the mRNA and protein expression of GSK‑3β, caspase‑3 and cyclin E. The potential mechanism of CUL4B highlighted in the present study may be helpful for the treatment of patients with gastric cancer.