Tan, Y., Sanders, Andrew J. ![]() ![]() ![]() |
Abstract
Background: IL-24, also termed MDA-7, is a member of the IL-10 family of cytokines. IL-24 is reported to be expressed in a series of cell lines, including keratinocytes as well as breast, lung and prostate cancer cells, but was primarily found in a human melanoma cell line. IL-24 is suggested to have many biological properties displaying anti-tumour effects via induction of apoptosis, suppressing proliferation, invasion and metastasis of cancer cells. IL-24 has also been reported to inhibit the migration of cancer cells and keratinocytes, and have anti-angiogeneic properties. The biological functions of IL-24 are regulated through both autocrine and paracrine methods. However, currently there exists little knowledge regarding the effect of IL-24 on endothelial cell biology. Materials and Methods: The impact of rhIL-24 on human endothelial HECV cell growth, migration, trans-endothelial resistance and angiogenic potential was examined using cellular functional assays. Additionally, the relationship between IL-24 and a number of cell junction proteins were examined using immunofluorescence staining. Results: IL-24 and receptor molecules was found to be expressed in HECV endothelial cells. Treatment of this cell line with rhIL-24 was found to promote cell migration rates and suppress tubule formation. Conclusion: Treatment of HECV cells with rhIL-24 can promote migration and inhibit tubule formation but does not impact cell growth or permeability at the tested concentrations. Potential links between IL-24 and AKT or PLCγ-related pathways with regard to these effects are also presented in the present study.
Item Type: | Article |
---|---|
Date Type: | Publication |
Status: | Published |
Schools: | Medicine |
Subjects: | R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer) |
Publisher: | International Institute of Anticancer Research |
ISSN: | 1109-6535 |
Last Modified: | 01 Nov 2022 09:29 |
URI: | https://orca.cardiff.ac.uk/id/eprint/88110 |
Citation Data
Cited 7 times in Scopus. View in Scopus. Powered By Scopus® Data
Actions (repository staff only)
![]() |
Edit Item |