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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.


The mRNA level of genes associated with cell cycle and apoptosis detected by qPCR. P27RF-Rho knockdown led to less expression of cyclin A, CDK2, MMP-9 and Bcl-2 mRNA. P27 and Bax mRNA levels increased after P27RF-Rho silencing
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f0003: The mRNA level of genes associated with cell cycle and apoptosis detected by qPCR. P27RF-Rho knockdown led to less expression of cyclin A, CDK2, MMP-9 and Bcl-2 mRNA. P27 and Bax mRNA levels increased after P27RF-Rho silencing

Mentions: Cell growth, apoptosis, and metastasis-associated genes were determined by quantitative PCR (Fig. 3). The results showed that the following mRNA levels were significantly lower in the P27RF-Rho-siRNA group than in the parental Bel7402 and negative control groups: cyclin A (0.38 ±0.06 vs. 2.75 ±0.48 and 2.76 ±0.42, p<0.01), CDK2 (0.59 ±0.16 vs. 4.19 ±0.48 and 4.09 ±0.52, p<0.01), MMP-9 (0.35 ±0.08 vs. 3.13 ±0.36 and 3.14 ±0.58, p<0.01), and BCL-2 (0.37 ±0.03 vs. 2.64 ±0.56 and 3.03 ±0.43, p<0.01). The following mRNA levels in the P27RF-Rho-siRNA group were notably increased when compared with the parental Bel7402 and negative control groups: P27 (1.13 ±0.13 vs. 0.19 ±0.04 and 0.18 ±0.06, p < 0.01) and BAX (1.04 ±0.09 vs. 0.12 ±0.03 and 0.11 ±0.03, p < 0.01).


Lentivirus-mediated knockdown of P27RF-Rho inhibits hepatocellular carcinoma cell growth
The mRNA level of genes associated with cell cycle and apoptosis detected by qPCR. P27RF-Rho knockdown led to less expression of cyclin A, CDK2, MMP-9 and Bcl-2 mRNA. P27 and Bax mRNA levels increased after P27RF-Rho silencing
© Copyright Policy - open-access
Related In: Results  -  Collection

License
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getmorefigures.php?uid=PMC5385476&req=5

f0003: The mRNA level of genes associated with cell cycle and apoptosis detected by qPCR. P27RF-Rho knockdown led to less expression of cyclin A, CDK2, MMP-9 and Bcl-2 mRNA. P27 and Bax mRNA levels increased after P27RF-Rho silencing
Mentions: Cell growth, apoptosis, and metastasis-associated genes were determined by quantitative PCR (Fig. 3). The results showed that the following mRNA levels were significantly lower in the P27RF-Rho-siRNA group than in the parental Bel7402 and negative control groups: cyclin A (0.38 ±0.06 vs. 2.75 ±0.48 and 2.76 ±0.42, p<0.01), CDK2 (0.59 ±0.16 vs. 4.19 ±0.48 and 4.09 ±0.52, p<0.01), MMP-9 (0.35 ±0.08 vs. 3.13 ±0.36 and 3.14 ±0.58, p<0.01), and BCL-2 (0.37 ±0.03 vs. 2.64 ±0.56 and 3.03 ±0.43, p<0.01). The following mRNA levels in the P27RF-Rho-siRNA group were notably increased when compared with the parental Bel7402 and negative control groups: P27 (1.13 ±0.13 vs. 0.19 ±0.04 and 0.18 ±0.06, p < 0.01) and BAX (1.04 ±0.09 vs. 0.12 ±0.03 and 0.11 ±0.03, p < 0.01).

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.