Premium
Role of anti‐angiogenic protein TSP‐1 in MAGE‐B2 driven cell proliferation
Author(s) -
Bagsby Clarke,
Colemon Ashley,
Ramanathan Saumya
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.06570
Subject(s) - cell growth , biology , microbiology and biotechnology , cancer research , signal transduction , effector , smad , somatic cell , gene , genetics
Melanoma Antigen Genes (MAGEs) are defined as cancer‐testis antigens due to their unique expression pattern. There are two families of MAGEs, Type I and Type II. Type I MAGEs are expressed in the testis and in no other normal somatic tissue and then re‐expressed in many cancers. Type II MAGEs on the other hand, are ubiquitous in their expression, meaning they are expressed in various somatic tissues. MAGE‐B2 is a member of the Type I subfamily. Expression of MAGE‐B2 causes increases in cell proliferation by as yet unknown mechanisms. Furthermore, depletion of MAGE‐B2 from cancer cells decreases cell proliferation. Our data indicate that the levels of anti‐angiogenic protein Thrombospondin‐1 (TSP‐1) is lowered in MAGE‐B2 expressing cells. TSP‐1 is also known as a regulator of TGFb signaling, because it activates TGFb. We will first determine whether TGFb signaling effectors such as TGFb, TGFb‐receptor, or Smad proteins are altered in expression and/or activity because of aberrant levels of MAGE‐B2. Then, we will determine whether TSP‐1 and TGFb signaling pathway effectors are needed for MAGE‐B2 driven proliferation, using gain and loss of function assays. In summary, these studies will shed light on the mechanisms that MAGE‐B2 uses to drive cell proliferation. Support or Funding Information NSF HBCU UP: Research Initiation Award HRD1764201 to S.R.