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[Effect and mechanism of VEGF antisense phosphorothioate deoxynucleotides on HL-60 leukemic cells]
1Institute of Hematology, Medical College of Jinan University, Guangzhou 510632, China.
Abstract:
To explore dose-effect or time-effect of vascular endothelial growth factor (VEGF) antisense phosphorothioate oligodeoxynucleotides (AS PS-ODN) on growth of HL-60 cells, and to study the effect mechanism so as to find new role of VEGF, A7, which was the most effective one of AS PS-ODN selected with computer-aided design and experimental assay, contains 20-DNA modified with phosphorothioate and was tranferred into cells mediated with lipofectin. After culture for 72 hours, inhibitive rate of cell growth was detected with MTT methods, viable cells were counted with trypan blue exclusion each 24 hour, cell configuration and apoptosis were observed with Geimsa staining and flow cytometry respectively, level of VEGF protein was detected with VEGF ELISA kit. The results showed that A7 is able to inhibit cell growth of HL-60 in dose-depending manner of AS PS-ODN, to down-regulate VEGF protein expression significantly, and not to induce apoptosis of HL-60 cells. It is concluded that there is possibility that the inhibition effect of VEGF AS PS-ODN on HL-60 cell growth is to restrain cell proliferation without inducing apoptosis of HL-60 cell, which would interpret that endogenous VEGF proteins have a capacity of promoting proliferation of HL-60 cell.
Insights
Vascular Endothelial Growth Factor (VEGF) antisense phosphorothioate oligodeoxynucleotides (AS PS-ODN) inhibit HL-60 cell growth by reducing proliferation, not inducing apoptosis. This suggests endogenous VEGF promotes HL-60 cell proliferation.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Context:
- The role of Vascular Endothelial Growth Factor (VEGF) in cancer progression is well-established.
- Investigating novel therapeutic strategies targeting VEGF signaling in leukemia is crucial.
Purpose:
- To explore the dose- and time-dependent effects of VEGF antisense phosphorothioate oligodeoxynucleotides (AS PS-ODN) on HL-60 cell growth.
- To elucidate the mechanism of action and identify a new role for VEGF in HL-60 cells.
Summary:
- A specific AS PS-ODN, A7, effectively inhibited HL-60 cell proliferation in a dose-dependent manner.
- A7 significantly downregulated VEGF protein expression without inducing apoptosis, as measured by MTT, trypan blue exclusion, Giemsa staining, and flow cytometry.
- VEGF protein levels were quantified using an ELISA kit.
Impact:
- This study suggests that inhibiting VEGF AS PS-ODN restrains HL-60 cell proliferation without inducing apoptosis.
- Findings indicate that endogenous VEGF may promote the proliferation of HL-60 cells, offering a potential therapeutic target.
