A review on the role of VEGF in Tamoxifen resistance.

Molecular deviations can contribute to the development of breast cancer. For instance, estrogen and estrogen receptors play a significant role in inducing tumor proliferation. However, the efficacy of endocrine therapy through administration of anti-estrogen drugs, such as Tamoxifen, is challenged by acquired resistance. Tamoxifen resistance occurs as a consequence of signaling pathways over-activated within this intricate network. Since angiogenesis is vital to tumor growth due to the essential nutrients it provides, it has been shown that microvessel count was greater in Tamoxifen resistant tissues than in responsive ones. Analyzing the molecular network involved in Tamoxifen resistance in breast cancer patients has depicted that the pathway triggered by vascular endothelial growth factor (VEGF) not only can cause angiogenesis, but can also facilitate proliferation of cancer cells. In this review, the interaction between estrogen, Tamoxifen, VEGF, and VEGFRs in Tamoxifen resistant cells has been discussed.