From: Recent updates of centromere proteins in hepatocellular carcinoma: a review
Interference tools | Centromere protein | Cell types | Main results | References |
---|---|---|---|---|
siRNA | CENP-A | HepG2 cells | Knockdown of CENP-A in HepG2 cells reduced cell proliferation, blocked cell cycle at the G1 phase, and increased apoptosis. | Li Y, et al.2011 |
siRNA (shCENPB#3) | CENP-B | Hep3B and MHCC97 cell lines | shCENPB#3 exhibited a significant inhibition of cell proliferation and invasion capacity in HCC cell lines upon downregulation of CENP-B expression. | Wang X, et al.2023 |
miR-29a | CENP-B | Hep3B and MHCC97 cell lines | miR-29a may act as a suppressor for HCC by negatively regulating CENP-B expression. | Wang X, et al.2023 |
GSK923295 | CENP-E | LM3, HUH7, and HepG2 cell lines | GSK923295 induced antiproliferation in HCC cell lines. Exposure of liver cells to GSK923295 resulted in delay on a cell cycle in mitosis with a phenotype of misaligned chromosomes and chromosomes clustered. | Tang JC, et al.2019 |
esiRNA (No. EHU047311) | CENP-F | HCCLM3 and Huh7 cells | CENP-F knockdown significantly inhibited the growth of HCCLM3 and Huh7 cells and inhibited Cyclin E1 and Cyclin B1 expression in HCC cells. | Chen H, et al.2022 |
double-stranded siRNAs | CENP-F | PLC8024 and SMMC7721 cells | Knockdown of CENP-F could also significantly reduce the abilities of HCC cells to form colonies, as evident in the foci formation assay. | Dai Y, et al.2013 |
siRNA | CENP-H | Hep3B cells | CENP-H knockdown suppressed the colony formation ability and induced apoptosis of the Hep3B cells. | Lu G, et al.2017 |
shRNA | CENP-K | BEL-7404 and SMMC-7721 cells | CENP-K downregulation inhibited cell viability and reduced the number of colonies formed by BEL-7404 and SMMC-7721 cells. Silencing CENP-K decreased the migration and invasion of HCC cells. | Wang J, et al.2019 |
miR-214-3p | CENP-M | Huh-7 and MHCC97-H cell lines | CENP-M mRNA and protein in HCC tissues was significant increased. miR-214-3p could negatively regulate the expression of CENP-M in HCC cells. | Zou Y, et al.2020 |
miRNA-214-3p | CENP-M | Huh7 and HepG2 cells | miRNA-214-3p distinctly suppressed the expressions of CENP-M, while its silence displayed an opposite result. | Ren H, et al.2021 |
si-CENPM | CENP-M | Huh7 and HepG2 cells | si-CENPM suppressed the expressions of CENP-M in Huh7 and HepG2 cells. Knockdown of CENP-M distinctly suppressed the proliferation, invasion and migration of Huh7 and HepG2 cells. | Ren H, et al.2021 |
si-CENPM | CENP-M | HepG2, SMMC-7721, LM3, MHCC-97Â H cells | Silencing CENP-M by si-CENP-M significantly suppressed the proliferation, migration and invasion ability of HCC cells. | Duan J, et al.2021 |
TMEM106C | CENP-M | HepG2, SMMC-7721, LM3, MHCC-97Â H cells | TMEM106C significantly suppressed the proliferation and metastasis of HCC through targeting CENP-M. | Duan J, et al.2021 |
siRNA (shRNA-CENPM) | CENP-M | Huh7 and HepG2 cells | Knocking down CENP-M inhibited cell proliferation, migration and invasion. Low-expression of CENP-M increased the proportion of cells in G2/M phase, and decreased the proportion of cells in G0/G1 both in Huh7 and HepG2 cell lines. | Xiao Y, et al.2019 |
siRNA | CENP-N | HepG2 and Huh7 | The expression of p53, p27, p21, CDK4, cyclin D1, CDK2, cyclin E, pRb, E2F1, and c-Myc decreased after CENP-N knockout. In addition, irradiated CENP-N knockout cells showed a significant increase in γ - H2AX expression and a decrease in colony formation. | Wang Q, et al.2021 |
siRNAs | CENP-U | Huh-7 and MHCC-97Â H cells | Knockdown of CENP-U inhibited the G1/S transition of HCC cells via E2F1. | Liu Y, et al.2022 |
siRNAs | CENP-W | Hep3B and Huh7 cells | Low expression of CENP-W was associated with better prognosis in HCC patients. SiRNA transfection could effectively knock out CENP-W in liver cancer cells. | Zhou Z, et al.2020 |
siRNAs | CENP-W | Hep3B and Huh7 cells | CENP-W knockdown could inhibit cell proliferation, migration and invasion by inducing the G0/G1 phase arrest and cell apoptosis in HCC cells via the E2F signaling regulation. | Zhou Y, et al.2021 |