Differential requirements for β-catenin in murine prostate cancer originating from basal versus luminal cells

Tsai Ling Lu, Chun Ming Chen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


A driver mutation occurring in different cells of origin may impact cancer progression differently. Previously, we demonstrated higher invasiveness in Pten-deficient prostate cancer (CaP) arising from basal cells compared to that arising from luminal cells in mice. Here, we show higher expression of epithelial-mesenchymal transition (EMT)-inducing transcription factors and stem/progenitor properties in basal-derived CaP compared to luminal-derived CaP. We further explore the requirement for β-catenin in basal and luminal prostate cells during CaP progression. Genetic ablation and pharmacological inhibition of β-catenin specifically suppress basal-derived CaP progression through reduction of stemness and cell proliferation and increased γH2Ax-associated apoptosis. Lineage tracing revealed that loss of β-catenin in basal cells impairs basal-to-luminal differentiation; conversely, β-catenin loss is dispensable for luminal-derived CaP progression. Our findings suggest that β-catenin is required for basal-derived normal luminal cells and cancer cells, but not for luminal derivatives. Although the cellular origin of CaP in patients cannot be easily determined at present, the results imply that β-catenin inhibition is a potential therapeutic option for a subset of patients with basal-derived CaP.

Original languageEnglish
Pages (from-to)290-301
Number of pages12
JournalJournal of Pathology
Issue number3
StatePublished - 1 Jul 2015


  • cell lineages
  • mouse model
  • prostate cancer
  • Pten


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