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Updated: Aug 30, 2026
In Vivo Imaging and Quantitation of the Host Angiogenic Response in Zebrafish Tumor Xenografts
Published on: August 14, 2019
Disruption of Id1 reveals major differences in angiogenesis between transplanted and autochthonous tumors
Hashmat Sikder1, David L Huso, Hong Zhang
1The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
Abstract:
Id genes regulate tumor angiogenesis and loss of Id1 inhibits tumor xenograft growth in mice. Here we evaluate the role of Id1 in a more clinically relevant tumor model system using a two-step chemical carcinogenesis protocol. Remarkably, we find that Id1-/- mice are more susceptible to skin tumorigenesis compared to their wild-type counterparts. Cutaneous neoplasms in Id1-/- mice show increased proliferation without alterations in tumor angiogenesis; however, Id1-/- mice possess 50% fewer cutaneous gammadelta T cells than their wild-type counterparts due to an intrinsic migration defect associated with loss of expression of the chemokine receptor, CXCR4. We suggest that there are important differences between the mechanisms of angiogenesis in transplanted and autochthonous tumors and that these findings will have significant implications for the potential utility of antiangiogenic therapies in cancer.
Insights
Loss of Id1 protein increases susceptibility to skin tumors in mice, with fewer T cells but no change in tumor angiogenesis. This suggests differences in tumor development mechanisms.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Id genes, including Id1, play a role in regulating tumor angiogenesis.
- Loss of Id1 has been shown to inhibit tumor xenograft growth in mice.
Purpose of the Study:
- To evaluate the role of Id1 in a more clinically relevant skin tumor model using chemical carcinogenesis.
- To investigate the impact of Id1 deficiency on skin tumorigenesis, proliferation, angiogenesis, and immune cell populations.
Main Methods:
- Utilized a two-step chemical carcinogenesis protocol in Id1 knockout (Id1-/-) and wild-type mice.
- Assessed tumor susceptibility, proliferation, and angiogenesis in cutaneous neoplasms.
- Quantified cutaneous gammadelta T cell populations and investigated chemokine receptor expression (CXCR4).
Main Results:
- Id1-/- mice exhibited increased susceptibility to skin tumorigenesis compared to wild-type counterparts.
- Cutaneous neoplasms in Id1-/- mice showed increased proliferation but no significant alterations in tumor angiogenesis.
- Id1-/- mice had 50% fewer cutaneous gammadelta T cells, linked to a migration defect from CXCR4 downregulation.
Conclusions:
- Id1 plays a protective role against chemical-induced skin tumorigenesis.
- Differences exist in angiogenesis mechanisms between transplanted and autochthonous tumors.
- Findings have implications for the efficacy of antiangiogenic therapies in cancer treatment.
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