Washington, Sept 30 : Scientists at the Kimmel Cancer Center at Jefferson in Philadelphia have found that prolactin, a pituitary hormone which stimulates breast development and milk production, initiates a new “signaling pathway” that may regulate the growth and survival of breast cancer cells.

The study, by Hallgeir Rui, M.D., Ph.D., professor of Cancer Biology at Jefferson Medical College of Thomas Jefferson University and Lynn Neilson, Ph.D., a postdoctoral fellow in the Department of Cancer Biology at Jefferson Medical College, identified the protein Jak1 as playing a key part in prolactin signaling in breast cancer.

“In breast cancer cells, we found that Jak1 not only stimulates conventional prolactin signaling via proteins such as Stat5, but also that Jak1 recruited new signals, especially Stat3 and ERK,” Rui said.

“Because Stat3 and ERK typically are considered tumor-promoting, inhibitors of Jak1 may become useful in breast cancer treatment,” he said.

Jak1 belongs to the cell growth-promoting tyrosine kinase class of enzymes, which could represent a new drug target for treating breast cancer.

Dr. Rui explained that the receptors for prolactin have previously been shown to promote breast cancer cell growth, survival, and differentiation, through signaling pathways that involved activation of such proteins as Stat5, ERK, and Akt.

In the current study, when Jak1 protein expression was experimentally disrupted in breast cancer cells, prolactin signaling through Stat3 and ERK was completely blocked. Also, signaling through Stat5 and Akt was reduced but still present.

“Until now, prolactin was believed to signal only through Jak2 to mediate its effects. The unexpected finding that prolactin also activates Jak1 in breast cancer points to a mechanism in cancer cells that further promotes tumor cell growth.” Lynn Neilson said.

The work is to appear in the journal Molecular Endocrinology. (With inputs from ANI)