Inhibition of TFAP2C reduced expression of two estrogen receptors and affected production of some downstream genes.

Transcription factor AP2C (TFAP2C) plays a central role in controlling multiple pathways of estrogen signaling in breast cancer, according to University of Iowa researchers.

The investigators report that silencing expression of TFAP2C in hormone-responsive breast cancer cells decreased the amount of ER-alpha made by the cancer cell. This reduction, which resulted in expression down to 16% of the level normally made by breast cancer cells, also affected production of other downstream genes involved in cancer growth.
In addition, silencing TFAP2C knocked out expression of another estrogen receptor called GPR30 that is found at the cancer cell membrane.

The Iowa team also say that these effects inhibited tumor growth. Specifically, the treated cancer cells did not grow in response to estrogen, and establishment of tumors in mice was delayed.

The findings were published in the September 15 issue of Cancer Research.

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