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Lentivirus-mediated knockdown of P27RF-Rho inhibits hepatocellular carcinoma cell growth

View Article: PubMed Central - PubMed

ABSTRACT

Aim of the study: To investigate the effects of P27RF-Rho on hepatocellular carcinoma (HCC) cell growth and explore the possibility of using it as a novel therapeutic target for liver cancer treatment.

Material and methods: P27RF-Rho in HCC cells was silenced by lentivirus-mediated RNA interference, and the silencing effect was verified by RT-PCR. Cell proliferation was determined by MTT and clone formation assay. Cell cycle phase and apoptosis were detected through FACS. The expression level of cell growth, apoptosis, and metastasis associated genes was detected by quantitative PCR.

Results: Lentivirus-mediated P27RF-Rho knockdown inhibited HCC cell growth and clone formation. P27RF-Rho silence induced cell cycle arrest and apoptosis. The mRNA level of genes associated with cell cycle, apoptosis, and invasion also significantly altered after P27RF-Rho knockdown. Cyclin A, CDK2, BCL-2, and MMP-9 were down-regulated. P27 and Bax were up-regulated.

Conclusions: P27RF-Rho knockdown inhibits HCC cell growth, and P27RF-Rho is probably a promising target for HCC treatment.

No MeSH data available.


Related in: MedlinePlus

Cell growth after P27Rf-Rho knockdown. A) P27Rf-Rho was knocked down by RNA interference. B) Cell growth was depressed after P27Rf-Rho knockdown. C) Cell clone formation inhibited by P27Rf-Rho silence
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f0001: Cell growth after P27Rf-Rho knockdown. A) P27Rf-Rho was knocked down by RNA interference. B) Cell growth was depressed after P27Rf-Rho knockdown. C) Cell clone formation inhibited by P27Rf-Rho silence

Mentions: The level of P27RF-Rho mRNA was significantly lower in the P27RF-Rho-siRNA group than in the parental Bel7402 and negative control groups (0.21 ±0.07 vs. 0.83 ±0.10, 0.88 ±0.12, p < 0.01). From the second day on, cell growth in the P27RF-Rho-siRNA group was remarkably slower than in the parental Bel7402 and negative control groups (0.44 ±0.01 vs. 0.62 ±0.03 and 0.60 ±0.04, p < 0.01). The clone formation ratio of cells in the P27RF-Rho-siRNA group was significantly lower than in the parental Bel7402 and negative control groups (13.50 ±1.73% vs. 49.83 ±6.43% and 47.17 ±4.04%, p<0.01), suggesting that P27RF-Rho-siRNA inhibited cell clone formation (Fig. 1).


Lentivirus-mediated knockdown of P27RF-Rho inhibits hepatocellular carcinoma cell growth
Cell growth after P27Rf-Rho knockdown. A) P27Rf-Rho was knocked down by RNA interference. B) Cell growth was depressed after P27Rf-Rho knockdown. C) Cell clone formation inhibited by P27Rf-Rho silence
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5385476&req=5

f0001: Cell growth after P27Rf-Rho knockdown. A) P27Rf-Rho was knocked down by RNA interference. B) Cell growth was depressed after P27Rf-Rho knockdown. C) Cell clone formation inhibited by P27Rf-Rho silence
Mentions: The level of P27RF-Rho mRNA was significantly lower in the P27RF-Rho-siRNA group than in the parental Bel7402 and negative control groups (0.21 ±0.07 vs. 0.83 ±0.10, 0.88 ±0.12, p < 0.01). From the second day on, cell growth in the P27RF-Rho-siRNA group was remarkably slower than in the parental Bel7402 and negative control groups (0.44 ±0.01 vs. 0.62 ±0.03 and 0.60 ±0.04, p < 0.01). The clone formation ratio of cells in the P27RF-Rho-siRNA group was significantly lower than in the parental Bel7402 and negative control groups (13.50 ±1.73% vs. 49.83 ±6.43% and 47.17 ±4.04%, p<0.01), suggesting that P27RF-Rho-siRNA inhibited cell clone formation (Fig. 1).

View Article: PubMed Central - PubMed

ABSTRACT

Aim of the study: To investigate the effects of P27RF-Rho on hepatocellular carcinoma (HCC) cell growth and explore the possibility of using it as a novel therapeutic target for liver cancer treatment.

Material and methods: P27RF-Rho in HCC cells was silenced by lentivirus-mediated RNA interference, and the silencing effect was verified by RT-PCR. Cell proliferation was determined by MTT and clone formation assay. Cell cycle phase and apoptosis were detected through FACS. The expression level of cell growth, apoptosis, and metastasis associated genes was detected by quantitative PCR.

Results: Lentivirus-mediated P27RF-Rho knockdown inhibited HCC cell growth and clone formation. P27RF-Rho silence induced cell cycle arrest and apoptosis. The mRNA level of genes associated with cell cycle, apoptosis, and invasion also significantly altered after P27RF-Rho knockdown. Cyclin A, CDK2, BCL-2, and MMP-9 were down-regulated. P27 and Bax were up-regulated.

Conclusions: P27RF-Rho knockdown inhibits HCC cell growth, and P27RF-Rho is probably a promising target for HCC treatment.

No MeSH data available.


Related in: MedlinePlus