September 13, 2018 Source: drugdu 57
The Jak2/Stat5 genetic pathway which controls the natural development of mammary glands and also breast cancer cells is regulated by the enzyme cyclophilin A (CypA), find VCU Massey Cancer Center researchers headed by Charles Clevenger, M.D., Ph.D., which could be a new target for breast cancer therapies.
"This research identifies cyclophilin A as a relevant target for therapeutic intervention in breast cancer. Because FDA-approved drugs are available to inhibit the action of CypA, translation of these findings to breast cancer patients should be rapid," said Clevenger, interim associate director for basic research, member of the Cancer Cell Signaling research program and Carolyn Wingate Endowed Chair in Cancer Research at VCU Massey Cancer Center. "No study to date had previously examined the loss of CypA function during mammary development and the formation of cancer."
Clevenger and his associates could suppress the initiation of the Stat5 pathway in mouse models having ER-positive and ER-negative breast cancer by obliterating the CypA enzyme. This resulted in the retardation or a complete stoppage in the development of breast cancer cells.
Earlier studies on prolactin receptor (PRLr) signaling helped in the spotting of CypA's involvement in the growth of breast cancer. A deeper analysis of the genetic pathways linked to PRLr signaling which considered Jak2 and Stat5 revealed that CypA was chiefly responsible for the initiation of the pathways.
"This study demonstrated many similarities to other loss-of-function mouse models of the PRL-PRLr-Jak2-Stat5 signaling pathway. However, what distinguishes the CypA-deprived mouse models from the other genetic deletion models was the mice's ability to still successfully lactate and nurse their offspring, despite the loss of an enzyme critical to mammary gland development," said Clevenger.
He thinks that the mice can continue to produce milk owing to the fact that the Jak2/Stat5 signaling pathways are either completely or majorly deactivated.By editor
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