E-cadherin: Its dysregulation in carcinogenesis and clinical implications

Sonia How Ming Wong, Chee Mun Fang, Lay Hong Chuah, Chee Onn Leong, Siew Ching Ngai

Research output: Contribution to journalReview ArticleOtherpeer-review

201 Citations (Scopus)


E-cadherin is a transmembrane glycoprotein which connects epithelial cells together at adherens junctions. In normal cells, E-cadherin exerts its tumour suppressing role mainly by sequestering β-catenin from its binding to LEF (Lymphoid enhancer factor)/TCF (T cell factor) which serves the function of transcribing genes of the proliferative Wnt signaling pathway. Despite the ongoing debate on whether the loss of E-cadherin is the cause or effect of epithelial-mesenchymal transition (EMT), E-cadherin functional loss has frequently been associated with poor prognosis and survival in patients of various cancers. The dysregulation of E-cadherin expression that leads to carcinogenesis happens mostly at the epigenetic level but there are cases of genetic alterations as well. E-cadherin expression has been linked to the cellular functions of invasiveness reduction, growth inhibition, apoptosis, cell cycle arrest and differentiation. Studies on various cancers have shown that these different cellular functions are also interdependent. Recent studies have reported a rapid expansion of E-cadherin clinical relevance in various cancers. This review article summarises the multifaceted effect E-cadherin expression has on cellular functions in the context of carcinogenesis as well as its clinical implications in diagnosis, prognosis and therapeutics.

Original languageEnglish
Pages (from-to)11-22
Number of pages12
JournalCritical Reviews in Oncology/Hematology
Publication statusPublished - Jan 2018


  • Apoptosis
  • Carcinogenesis
  • Dysregulation
  • E-cadherin
  • Invasiveness

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