The role of IL17B-IL17RB signaling pathway in breast cancer.
Breast cancer is the most important cause of death in women globally. Though, improved survival is due to the developments in the screening techniques, initial diagnosis, and advances in treatments. Numerous factors contributed in the progression of breast cancer, such as inflammation. The most significant factor involved in the inflammatory process, is T helper 17 (Th17) cells. Th17 cells have an exceptional role in many of inflammatory diseases like psoriasis, rheumatoid arthritis, and breast cancer through production of proinflammatory cytokine (IL17). As the collected indication recommends a possible relevance between chronic inflammation and cancer tumorigenesis, it appears that this cytokine can stimulate the tumorigenesis of breast tumor cells. The IL17 family consist of 6 protein members, among them IL17B and its receptor, and IL17RB signaling pathway plays a key role in development and progression of breast cancer, and targeting this signaling pathway or its specific downstream mediators by a chemotherapy drug and small interfering RNA interference is a potentially novel therapeutic pathway for inhibition of this disease. This comprehensive review details the recognition of activity, signaling, and the roles of IL17B-IL17RB in breast cancer have caused to determination of new therapeutic mechanisms with the purpose of introduction this system and the regulation of its signaling pathway.
Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Vahideh
V
Alinejad
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Sanam
S
Dolati
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Morteza
M
Motallebnezhad
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: Yousefime@tbzmed.ac.ir.
Mehdi
M
Yousefi
D000818:Animals; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism; D005260:Female; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism; D020381:Interleukin-17 / Q000235:genetics* / Q000378:metabolism; D018123:Receptors, Interleukin / Q000235:genetics* / Q000378:metabolism; D053722:Receptors, Interleukin-17; D015398:Signal Transduction; D058504:Th17 Cells / Q000378:metabolism
C515924:IL17B protein, human; C408922:IL17RB protein, human; D020381:Interleukin-17; D018123:Receptors, Interleukin; D053722:Receptors, Interleukin-17
Breast cancer; IL17B; IL17RB