TY - JOUR
T1 - Epithelial protein lost in neoplasm (EPLIN)
T2 - Beyond a tumor suppressor
AU - Wu, Daqing
N1 - Funding Information:
This work was supported by National Cancer Institute grants 1R21CA164612-01A1, 1R41CA186498-01A1 and 1R41CA206725-01A1, Georgia Research Alliance Ventures grant, University of Georgia/Augusta University Cancer Research Initiative Award, and Georgia Cancer Center Startup Fund (D. Wu). We thank Dr. Rhea-Beth Markowitz for editorial assistance.
Publisher Copyright:
© 2017 Chongqing Medical University
PY - 2017/6
Y1 - 2017/6
N2 - The majority of cancer-related deaths are caused by tumor recurrence, metastasis and therapeutic resistance. During the late stages of tumor progression, multiple factors are involved, including the downregulation and/or loss of function of metastasis suppressors. Epithelial protein lost in neoplasm (EPLIN), an actin-binding protein, was initially identified as a putative tumor suppressor that is frequently downregulated in epithelial tumors. Recent evidence indicates that EPLIN may negatively regulate epithelia-to-mesenchymal transition (EMT), a crucial process by which cancer cells acquire invasive capabilities and therapeutic resistance. Importantly, downregulation of EPLIN is associated with clinical metastasis in a variety of solid tumors, suggesting that EPLIN could be a suppressor of metastasis. In this review, I will discuss the regulation and function of EPLIN in human cancer cells and explore the clinical significance of EPLIN in metastatic disease.
AB - The majority of cancer-related deaths are caused by tumor recurrence, metastasis and therapeutic resistance. During the late stages of tumor progression, multiple factors are involved, including the downregulation and/or loss of function of metastasis suppressors. Epithelial protein lost in neoplasm (EPLIN), an actin-binding protein, was initially identified as a putative tumor suppressor that is frequently downregulated in epithelial tumors. Recent evidence indicates that EPLIN may negatively regulate epithelia-to-mesenchymal transition (EMT), a crucial process by which cancer cells acquire invasive capabilities and therapeutic resistance. Importantly, downregulation of EPLIN is associated with clinical metastasis in a variety of solid tumors, suggesting that EPLIN could be a suppressor of metastasis. In this review, I will discuss the regulation and function of EPLIN in human cancer cells and explore the clinical significance of EPLIN in metastatic disease.
KW - Actin cytoskeleton
KW - Chemoresistance
KW - EPLIN
KW - Epithelial-to-mesenchymal transition
KW - Metastasis suppressor
KW - Tumor suppressor
UR - http://www.scopus.com/inward/record.url?scp=85017553629&partnerID=8YFLogxK
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U2 - 10.1016/j.gendis.2017.03.002
DO - 10.1016/j.gendis.2017.03.002
M3 - Review article
AN - SCOPUS:85017553629
SN - 2352-4820
VL - 4
SP - 100
EP - 107
JO - Genes and Diseases
JF - Genes and Diseases
IS - 2
ER -
