Retracted: Effects of cyclin D1 gene silencing on cell proliferation, cell cycle, and apoptosis of hepatocellular carcinoma cells

Abstract

This study aims to investigate the effects of Cyclin D1 silencing on cell cycle, cell proliferation, and apoptosis of hepatocellular carcinoma cells (HCC). Cells were divided into the blank group, negative control group (HCC cells transfected with control shRNA), Cyclin D1 shRNA group (HCC cells transfected with Cyclin D1 shRNA), and the normal group (human normal liver L-02 cells). Expressions of Cyclin D1, Caspase-3, Bcl-2, and C-myc were detected by RT-qPCR and Western blotting. Cell proliferation was detected by Cell Counting Kit-8. Cell cycle and apoptosis were detected by flow cytometry. Tumor xenograft in nude mice was performed to detect in vivo tumorigenesis. HCC tissues and HCC cells exhibited elevated expression levels of Cyclin D1. Cyclin D1 expression levels was found to be correlated with tumor size and tumor staging. Compared with the normal group, the blank group showed enhanced cell proliferation, a reduction in the amount of cells in G0/G1 phase, increased number cells in S and G2/M phase, reduced apoptosis, elevated expressions of Cyclin D1, Bcl-2, and C-myc, decreased Caspase-3 activity and significant tumorigenicity. In comparison with the blank group, the Cyclin D1 shRNA group revealed weakened cell proliferation, reduced cells in S and G2/M phase, increased cells in G0/G1 phase, increased Annexin V positive cell ratio, decreased expression of Cyclin D1, Bcl-2, and C-myc, elevated Caspase-3 activity and inhibited tumorigenicity. In conclusion, Cyclin D1 gene silencing suppresses cell proliferation and inhibits cell apoptosis, which may be a new target approach in the treatment and management for HCC.

Amentoflavone Inhibits Hepatocellular Carcinoma Progression Through Blockage of ERK/NF-ĸB Activation

“…Cyclin-D1, a regulator of cell cycle at the G 1 to S transition, was also overexpressed in HCC tissues. High expression of cyclin-D1 was also correlated with tumor stage in HCC (19). Silencing of C-FLIP, XIAP, cyclin-D1, or MCL-1 by small interfering ribonucleic acid (siRNA) or short hairpin RNA inhibited cell proliferation and triggered apoptosis in HCC cell lines (4,6,20).…”

Upregulated calcium‐binding tyrosine phosphorylation‐regulated protein‐a/b regulates cell proliferation and apoptosis and predicts poor prognosis in hepatocellular carcinoma

“…Cyclin D1, belonging to the highly conserved cyclin family, forms an active complex with CDK4 or CDK6 to drive cell cycle transition from G1 to the S phase . Overexpression of cyclin D1 or hyperactivation of CDK4 directly result in dysregulation of cell cycle and cell proliferation .…”

“…Cyclin D1, belonging to the highly conserved cyclin family, forms an active complex with CDK4 or CDK6 to drive cell cycle transition from G1 to the S phase. 22,23 Overexpression of cyclin D1 or hyperactivation of CDK4 directly result in dysregulation of cell cycle and cell proliferation. 23,24 Our data show that CABYR-a/b knockdown leads to an increased ratio of cells in G0/G1 phase, suppression of cell proliferation, and downregulation of cyclin D1 and CDK4, suggesting that CABYR-a/b downregulation affects HCC cell proliferation by regulating cyclin D1 and CDK4 levels.…”

Epigenetic knockdown of Notch1 inhibits hepatitis B virus X protein‑induced hepatocarcinogenesis of L02/HBx cells

“…Kunter et al confirmed that inhibition of PI3K/Akt signaling could arrest HCC cells at the G 0 /G 1 phase by regulating Rb/E2F1 (40). Chen et al indicated that silencing of cyclin D1 could arrest HCC cells in the G 0 /G 1 phase (41). In addition, CDK4 was found to be enzymatically activated by D-type cyclins to inactivate retinoblastoma, and thus arrest G1/S transition (42).…”