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Effect of vascular endothelial growth factor siRNA and wild‑type p53 co‑expressing plasmid in MDA‑MB‑231 cells
Hua Guo1, Yang Li1, Junlian Gu2
1Department of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, Norman Bethune College of Medicine, Jilin University, Changchun, Jilin 130021, P.R. China.
Abstract:
Breast cancer urgently requires improved therapeutic strategies. In the current study, a Pvp53 plasmid that co‑expressed p53 and short‑interfering RNA against vascular endothelial growth factor (si‑VEGF) was developed to replace single plasmid transfections. Whether Pvp53 exhibited improved anti‑tumor effects in breast cancer MDA‑MB‑231 cells was investigated in the present study. Pvp53 significantly reduced the Bcl‑2/Bax ratio and increased the expression of cleaved caspase‑3 and 8. Compared with p53 and si‑VEGF single transfections, the Pvp53 co‑expression plasmid significantly increased the proportion of apoptotic cells and inhibited cell motility and proliferation. These results indicated that the Pvp53 co‑expression plasmid has greater inhibitory effects on breast cancer MDA‑MB‑231 cells than single plasmids.
Insights
A novel Pvp53 plasmid co-expressing p53 and short-interfering RNA against vascular endothelial growth factor (si-VEGF) demonstrated enhanced anti-tumor effects in breast cancer cells. This combined approach significantly boosted apoptosis and inhibited tumor cell growth more effectively than single plasmid treatments.
Area of Science:
- Oncology
- Molecular Biology
- Gene Therapy
Background:
- Breast cancer necessitates advanced therapeutic approaches.
- Current treatments often involve single-gene targeting, which may limit efficacy.
- Developing combination therapies can potentially overcome treatment resistance and improve outcomes.
Purpose of the Study:
- To evaluate the anti-tumor efficacy of a novel co-expression plasmid (Pvp53) in breast cancer cells.
- To compare the effects of Pvp53, which expresses p53 and short-interfering RNA against vascular endothelial growth factor (si-VEGF), against single plasmid transfections.
- To investigate the molecular mechanisms underlying Pvp53's anti-cancer activity.
Main Methods:
- Construction and transfection of the Pvp53 co-expression plasmid into MDA-MB-231 breast cancer cells.
- Assessment of apoptosis-related protein expression, including Bcl-2/Bax ratio and cleaved caspase-3 and -8.
- Evaluation of cell proliferation, motility, and apoptosis rates.
Main Results:
- Pvp53 significantly modulated the Bcl-2/Bax ratio, indicating an apoptotic pathway activation.
- Co-expression of p53 and si-VEGF via Pvp53 led to increased cleaved caspase-3 and -8 levels.
- The Pvp53 plasmid demonstrated a superior ability to induce apoptosis and inhibit cell motility and proliferation compared to single p53 or si-VEGF plasmids.
Conclusions:
- The Pvp53 co-expression plasmid exhibits enhanced anti-tumor effects on MDA-MB-231 breast cancer cells.
- Combined expression of p53 and si-VEGF offers a more potent therapeutic strategy than individual gene targeting.
- Pvp53 holds promise as an improved therapeutic agent for breast cancer treatment.
