Anti-Müllerian Hormone Signaling Regulates Epithelial Plasticity and Chemoresistance in Lung Cancer
Genre
Journal articleDate
2016-07-19Author
Beck, Tim N.Korobeynikov, Vladislav A.
Kudinov, Alexander E.
Georgopoulos, Rachel
Solanki, Nehal R.
Andrews-Hoke, Magda
Kistner, Timothy M.
Pépin, David
Donahoe, Patricia K.
Nicolas, Emmanuelle
Einarson, Margret B.
Zhou, Yan
Boumber, Yanis

Proia, David A.
Serebriiskii, Ilya G.
Golemis, Erica

Group
Fox Chase Cancer Center (Temple University)Department
Cancer and Cellular BiologyPermanent link to this record
http://hdl.handle.net/20.500.12613/9186
Metadata
Show full item recordDOI
http://dx.doi.org/10.1016/j.celrep.2016.06.043Abstract
Anti-Müllerian hormone (AMH) and its type II receptor AMHR2, both previously thought to primarily function in gonadal tissue, were unexpectedly identified as potent regulators of transforming growth factor (TGF-β)/bone morphogenetic protein (BMP) signaling and epithelial-mesenchymal transition (EMT) in lung cancer. AMH is a TGF-β/BMP superfamily member, and AMHR2 heterodimerizes with type I receptors (ALK2, ALK3) also used by the type II receptor for BMP (BMPR2). AMH signaling regulates expression of BMPR2, ALK2, and ALK3, supports protein kinase B-nuclear factor κB (AKT-NF-κB) and SMAD survival signaling, and influences BMP-dependent signaling in non-small cell lung cancer (NSCLC). AMH and AMHR2 are selectively expressed in epithelial versus mesenchymal cells, and loss of AMH/AMHR2 induces EMT. Independent induction of EMT reduces expression of AMH and AMHR2. Importantly, EMT associated with depletion of AMH or AMHR2 results in chemoresistance but sensitizes cells to the heat shock protein 90 (HSP90) inhibitor ganetespib. Recognition of this AMH/AMHR2 axis helps to further elucidate TGF-β/BMP resistance-associated signaling and suggests new strategies for therapeutic targeting of EMT.Citation
Beck TN, Korobeynikov VA, Kudinov AE, Georgopoulos R, Solanki NR, Andrews-Hoke M, et al. Anti-Müllerian Hormone Signaling Regulates Epithelial Plasticity and Chemoresistance in Lung Cancer. Cell Rep. 2016 Jul 19;16(3):657-671. doi:10.1016/j.celrep.2016.06.043.Citation to related work
Cell PressHas part
Cell Reports, Vol. 16, Iss. 3ADA compliance
For Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.eduCollections
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs CC BY-NC-ND