Identifying novel drug targets that differentiate cancer cells from healthy ones is key to developing precise and effective treatments for breast cancer.
In the Aug. 15 issue of Cancer Research, Barbara Fingleton, Ph.D., and colleagues demonstrate that the interaction between the cytokine interleukin 4 (IL4) and a subunit of its receptor, the IL4R-alpha chain, promotes mammary metastatic tumor growth. Silencing IL4R-alpha expression significantly reduced epithelial cancer cell survival and proliferation in cultured human breast cancer cells, as well as metastatic tumor mass in lung and liver in a mouse cancer model. Similar results were observed in IL4-deficient mice.
Targeting IL4/IL4R-alpha signaling in epithelial cancer cells thus may be a way to inhibit breast cancer cell survival and metastasis. However, it would be important not to block IL4R signaling in immune cells that have potential anti-tumor functions.
The advent of pharmaceutical “superkines” highly specific for tumor cell IL4Rs may open the door for a novel targeted treatment, the researchers concluded.
This research was supported by grants from the Department of Defense and the National Institutes of Health (CA157781, GM008554, CA068485, TR000445).
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