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Apurinic/apyrimidinic endonuclease 1 induced upregulation of fibroblast growth factor 2 and its receptor 3 induces angiogenesis in human osteosarcoma cells.

Ren T, Qing Y, Dai N, Li M, Qian C, Yang Y, Cheng Y, Li Z, Zhang S, Zhong Z, Wang D - Cancer Sci. (2014)

Bottom Line: Our preliminary data show small interfering RNA-mediated silence of APE1 experiments, which further supports this hypothesis.APE1-small interfering RNA significantly inhibited tumor angiogenesis by downregulating in vitro expression of FGF2 and FGFR3 in human umbilical vein endothelial cells in Matrigel tube formation assay, and further inhibited tumor growth in vivo in a mouse xenograft model.Thus, the proposed APE1-FGF2 and FGFR3 pathway may provide a novel mechanism for regulation of FGF2 and FGFR3 by APE1 in tumor angiogenesis.

View Article: PubMed Central - PubMed

Affiliation: Cancer Center, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing, China.

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Apurinic/apyrimidinic endonuclease 1 (APE1)-siRNA suppresses the capacity of tumor cells to promote HUVEC migration in a transwell model and tube formation in a Matrigel-based angiogenesis assay. (a) Representative images of migration are presented. Compared to the control, fewer HUVEC were migrated in the lower compartment filled with culture medium that contained APE1-siRNA treated 9901 cells. The migration capacity of the culture medium containing 9901 cells treated with 0.3 nMAPE1-siRNA in the lower compartment was largely restored by an addition of recombinant FGF2. (b) Quantitative analysis of HUVEC migration. (c) HUVEC were cultured in 24-well plates coated with Matrigel in tumor-condition medium (TCM) derived from 9901 cells without transfection or cells were transfected with APE1-siRNA. Representative images of tube formation are presented. In the presence of TCM derived from HUVEC transfected with APE1-siRNA, these cells developed fewer capillary-like structures compared to the control. The angiogenic capacity of the TCM derived from 0.3 nM APE1-siRNA transfected cells was promoted by an addition of recombinant FGF2. (d) Quantitative analysis of HUVEC angiogenesis. Data are represented as mean ± SD (n = 3, **P < 0.01).
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fig04: Apurinic/apyrimidinic endonuclease 1 (APE1)-siRNA suppresses the capacity of tumor cells to promote HUVEC migration in a transwell model and tube formation in a Matrigel-based angiogenesis assay. (a) Representative images of migration are presented. Compared to the control, fewer HUVEC were migrated in the lower compartment filled with culture medium that contained APE1-siRNA treated 9901 cells. The migration capacity of the culture medium containing 9901 cells treated with 0.3 nMAPE1-siRNA in the lower compartment was largely restored by an addition of recombinant FGF2. (b) Quantitative analysis of HUVEC migration. (c) HUVEC were cultured in 24-well plates coated with Matrigel in tumor-condition medium (TCM) derived from 9901 cells without transfection or cells were transfected with APE1-siRNA. Representative images of tube formation are presented. In the presence of TCM derived from HUVEC transfected with APE1-siRNA, these cells developed fewer capillary-like structures compared to the control. The angiogenic capacity of the TCM derived from 0.3 nM APE1-siRNA transfected cells was promoted by an addition of recombinant FGF2. (d) Quantitative analysis of HUVEC angiogenesis. Data are represented as mean ± SD (n = 3, **P < 0.01).

Mentions: To explore the biological significance of the silencing of APE1 upregulated FGF2 and FGFR3 expression in tumor angiogenesis, transwell migration assays were carried out in HUVEC. As shown in Figure 4(a,b), a smaller number of HUVEC was migrated in the 0.3 nM APE1-siRNA treatment group than in the control group (36.20 ± 4.76 vs 113.20 ± 4.97, P < 0.0001) and, unexpectedly, this reduced migration activity was largely restored by an addition of recombinant FGF2 (58.80 ± 8.35 vs 36.20 ± 4.76, P = 0.0008). Furthermore, Matrigel tube formation assays carried out in HUVEC using TCM showed formation of fewer capillary tubes in the presence of TCM derived from cells with APE1-siRNA (0.3 nM) in a dose-dependent manner as compared to the control group (1.80 ± 0.84 vs 28.00 ± 5.83, P < 0.0001; Fig. 4c,d). Similarly, this reduced angiogenic capacity of the TCM was mostly restored with an addition of recombinant FGF2 (8.60 ± 2.70 vs 1.80 ± 0.84, P = 0.0007; Fig. 4c,d).


Apurinic/apyrimidinic endonuclease 1 induced upregulation of fibroblast growth factor 2 and its receptor 3 induces angiogenesis in human osteosarcoma cells.

Ren T, Qing Y, Dai N, Li M, Qian C, Yang Y, Cheng Y, Li Z, Zhang S, Zhong Z, Wang D - Cancer Sci. (2014)

Apurinic/apyrimidinic endonuclease 1 (APE1)-siRNA suppresses the capacity of tumor cells to promote HUVEC migration in a transwell model and tube formation in a Matrigel-based angiogenesis assay. (a) Representative images of migration are presented. Compared to the control, fewer HUVEC were migrated in the lower compartment filled with culture medium that contained APE1-siRNA treated 9901 cells. The migration capacity of the culture medium containing 9901 cells treated with 0.3 nMAPE1-siRNA in the lower compartment was largely restored by an addition of recombinant FGF2. (b) Quantitative analysis of HUVEC migration. (c) HUVEC were cultured in 24-well plates coated with Matrigel in tumor-condition medium (TCM) derived from 9901 cells without transfection or cells were transfected with APE1-siRNA. Representative images of tube formation are presented. In the presence of TCM derived from HUVEC transfected with APE1-siRNA, these cells developed fewer capillary-like structures compared to the control. The angiogenic capacity of the TCM derived from 0.3 nM APE1-siRNA transfected cells was promoted by an addition of recombinant FGF2. (d) Quantitative analysis of HUVEC angiogenesis. Data are represented as mean ± SD (n = 3, **P < 0.01).
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fig04: Apurinic/apyrimidinic endonuclease 1 (APE1)-siRNA suppresses the capacity of tumor cells to promote HUVEC migration in a transwell model and tube formation in a Matrigel-based angiogenesis assay. (a) Representative images of migration are presented. Compared to the control, fewer HUVEC were migrated in the lower compartment filled with culture medium that contained APE1-siRNA treated 9901 cells. The migration capacity of the culture medium containing 9901 cells treated with 0.3 nMAPE1-siRNA in the lower compartment was largely restored by an addition of recombinant FGF2. (b) Quantitative analysis of HUVEC migration. (c) HUVEC were cultured in 24-well plates coated with Matrigel in tumor-condition medium (TCM) derived from 9901 cells without transfection or cells were transfected with APE1-siRNA. Representative images of tube formation are presented. In the presence of TCM derived from HUVEC transfected with APE1-siRNA, these cells developed fewer capillary-like structures compared to the control. The angiogenic capacity of the TCM derived from 0.3 nM APE1-siRNA transfected cells was promoted by an addition of recombinant FGF2. (d) Quantitative analysis of HUVEC angiogenesis. Data are represented as mean ± SD (n = 3, **P < 0.01).
Mentions: To explore the biological significance of the silencing of APE1 upregulated FGF2 and FGFR3 expression in tumor angiogenesis, transwell migration assays were carried out in HUVEC. As shown in Figure 4(a,b), a smaller number of HUVEC was migrated in the 0.3 nM APE1-siRNA treatment group than in the control group (36.20 ± 4.76 vs 113.20 ± 4.97, P < 0.0001) and, unexpectedly, this reduced migration activity was largely restored by an addition of recombinant FGF2 (58.80 ± 8.35 vs 36.20 ± 4.76, P = 0.0008). Furthermore, Matrigel tube formation assays carried out in HUVEC using TCM showed formation of fewer capillary tubes in the presence of TCM derived from cells with APE1-siRNA (0.3 nM) in a dose-dependent manner as compared to the control group (1.80 ± 0.84 vs 28.00 ± 5.83, P < 0.0001; Fig. 4c,d). Similarly, this reduced angiogenic capacity of the TCM was mostly restored with an addition of recombinant FGF2 (8.60 ± 2.70 vs 1.80 ± 0.84, P = 0.0007; Fig. 4c,d).

Bottom Line: Our preliminary data show small interfering RNA-mediated silence of APE1 experiments, which further supports this hypothesis.APE1-small interfering RNA significantly inhibited tumor angiogenesis by downregulating in vitro expression of FGF2 and FGFR3 in human umbilical vein endothelial cells in Matrigel tube formation assay, and further inhibited tumor growth in vivo in a mouse xenograft model.Thus, the proposed APE1-FGF2 and FGFR3 pathway may provide a novel mechanism for regulation of FGF2 and FGFR3 by APE1 in tumor angiogenesis.

View Article: PubMed Central - PubMed

Affiliation: Cancer Center, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing, China.

Show MeSH
Related in: MedlinePlus