Amyloid precursor protein and amyloid precursor-like protein 2 in cancer
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Poomy Pandey1, Bailee Sliker1, Haley L. Peters1,6, Amit Tuli1,2,7, Jonathan Herskovitz1, Kaitlin Smits1, Abhilasha Purohit3, Rakesh K. Singh3,4, Jixin Dong1,4, Surinder K. Batra2,4, Donald W. Coulter4,5 and Joyce C. Solheim1,2,3,4
1 Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA
2 Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA
3 Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA
4 Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, USA
5 Department of Pediatrics, University of Nebraska Medical Center, Omaha, NE, USA
6 Department of Stem Cell Transplantation and Cellular Therapy, University of Texas MD Anderson Cancer Center, Houston, TX, USA
7 Wellcome Trust/DBT India Alliance Intermediate Fellow, CSIR-Institute of Microbial Technology, Chandigarh, India
Joyce C. Solheim, email:
Keywords: amyloid precursor protein, amyloid precursor-like protein 2, cancer, growth, migration
Received: October 02, 2015 Accepted: January 23, 2016 Published: January 31, 2016
Amyloid precursor protein (APP) and its family members amyloid precursor-like protein 1 (APLP1) and amyloid precursor-like protein 2 (APLP2) are type 1 transmembrane glycoproteins that are highly conserved across species. The transcriptional regulation of APP and APLP2 is similar but not identical, and the cleavage of both proteins is regulated by phosphorylation. APP has been implicated in Alzheimer’s disease causation, and in addition to its importance in neurology, APP is deregulated in cancer cells. APLP2 is likewise overexpressed in cancer cells, and APLP2 and APP are linked to increased tumor cell proliferation, migration, and invasion. In this present review, we discuss the unfolding account of these APP family members’ roles in cancer progression and metastasis.
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