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E2F-1 overexpression inhibits human gastric cancer MGC-803 cell growth in vivo
Wei-Yuan Wei1, Lin-Hai Yan1, Xiao-Tong Wang1
1Wei-Yuan Wei, Lin-Hai Yan, Wen-Long Cao, Xiao-Shi Zhang, Ze-Xu Zhan, Han Yu, Qiang Xiao, Department of Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China.
Aim:
To evaluate the influence of E2F-1 on the growth of human gastric cancer (GC) cells in vivo and the mechanism involved.
Methods:
E2F-1 recombinant lentiviral vectors were injected into xenograft tumors of MGC-803 cells in nude mice, and then tumor growth was investigated. Overexpression of transcription factor E2F-1 was assessed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting analysis. Apoptosis rates were determined using a terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay. Expression levels of certain cell cycle regulators and apoptosis-related proteins, such as Bax, survivin, Bcl-2, cyclin D1, S-phase kinase-associated protein 2, and c-Myc were examined by Western blotting and RT-PCR.
Results:
Xenograft tumors of MGC-803 cells in nude mice injected with E2F-1 recombinant lentiviral vectors stably overexpressed the E2F-1 gene as measured by semi-quantitative RT-PCR (relative mRNA expression: 0.10 ± 0.02 vs 0.05 ± 0.02 for control vector and 0.06 ± 0.03 for no infection; both P < 0.01) and Western blotting (relative protein expression: 1.90 ± 0.05 vs 1.10 ± 0.03 in control vector infected and 1.11 ± 0.02 for no infection; both P < 0.01). The growth-curve of tumor volumes revealed that infection with E2F-1 recombinant lentiviral vectors significantly inhibited the growth of human GC xenografts (2.81 ± 1.02 vs 6.18 ± 1.15 in control vector infected and 5.87 ± 1.23 with no infection; both P < 0.05) at 15 d after treatment. TUNEL analysis demonstrated that E2F-1 overexpression promoted tumor cell apoptosis (18.6% ± 2.3% vs 6.7% ± 1.2% in control vector infected 6.3% ± 1.2% for no infection; both P < 0.05). Furthermore, lentiviral vector-mediated E2F-1 overexpression increased the expression of Bax and suppressed survivin, Bcl-2, cyclin D1, Skp2, and c-Myc expression in tumor tissue.
Conclusion:
E2F-1 inhibits growth of GC cells via regulating multiple signaling pathways, and may play an important role in targeted therapy for GC.
Insights
Overexpressing E2F-1 in human gastric cancer cells significantly inhibited tumor growth and promoted apoptosis. This suggests E2F-1 may be a potential target for gastric cancer therapy.
Area of Science:
- Oncology
- Molecular Biology
- Gene Therapy
Background:
- Gastric cancer (GC) remains a significant global health challenge.
- Understanding the molecular mechanisms regulating GC growth is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the role of the transcription factor E2F-1 in human gastric cancer (GC) cell growth in vivo.
- To elucidate the underlying molecular mechanisms by which E2F-1 influences GC progression.
Main Methods:
- Utilized E2F-1 recombinant lentiviral vectors for gene overexpression in MGC-803 GC xenografts in nude mice.
- Assessed E2F-1 expression via RT-PCR and Western blotting.
- Quantified apoptosis rates using TUNEL assay.
- Examined expression of cell cycle and apoptosis-related proteins (Bax, survivin, Bcl-2, cyclin D1, Skp2, c-Myc).
Main Results:
- Stable E2F-1 overexpression was confirmed in xenograft tumors.
- E2F-1 overexpression significantly inhibited tumor growth and increased apoptosis rates.
- Increased expression of Bax and decreased expression of survivin, Bcl-2, cyclin D1, Skp2, and c-Myc were observed.
Conclusions:
- E2F-1 inhibits gastric cancer cell growth through the regulation of multiple signaling pathways.
- E2F-1 demonstrates potential as a therapeutic target for gastric cancer treatment.
