Epithelial protein lost in neoplasm (EPLIN): Beyond a tumor suppressor

Daqing Wu

Research output: Contribution to journalReview articlepeer-review

10 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)100-107
Number of pages8
JournalGenes and Diseases
Issue number2
StatePublished - Jun 2017
Externally publishedYes


  • Actin cytoskeleton
  • Chemoresistance
  • Epithelial-to-mesenchymal transition
  • Metastasis suppressor
  • Tumor suppressor

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics(clinical)
  • Cell Biology


Dive into the research topics of 'Epithelial protein lost in neoplasm (EPLIN): Beyond a tumor suppressor'. Together they form a unique fingerprint.

Cite this