SFRP1 inhibited epithelial ovarian cancer through inhibiting Wnt/β-catenin pathway, suggesting that SFRP1 could be considered as a potential therapeutic target in epithelial ovarian cancer.
Protein tyrosine phosphatase receptor type R (PTPRR) antagonizes the Wnt signaling pathway in ovarian cancer by dephosphorylating and inactivating β-catenin.
Further, the expression of SOX9, β-catenin, and c-Myc in OC tissues was upregulated and inversely correlated with miR-34c expression, indicating that rescuing miR-34c expression, thus to inhibit SOX9, β-catenin, and c-Myc expression presents a promising strategy of reducing the chemoresistance of the OC cell to DDP.
Moreover, combined inhibition of PARP and Wnt/β-catenin showed synergistic suppression of PARPi-resistant cells <i>in vitro</i> and <i>in vivo</i> in a xenograft EOC mouse model.
Glutamine-fructose-6-phosphate transaminase 2 (GFPT2) promotes the EMT of serous ovarian cancer by activating the hexosamine biosynthetic pathway to increase the nuclear location of β-catenin.
To establish immunohistochemical (IHC) panels for prognosis prediction of OECa for use in daily pathology practice, the expression patterns of 12 IHC markers, p53, HNF-1β, ARID1A, estrogen receptor-α, progesterone receptor, vimentin, PTEN, PIK3CA, WT1, left-right determination factor, β-catenin, and Ki-67 were investigated using 282 OECas.
Nucleus and/or cytoplasma of β-catenin expression might be associated with tumor progression and could be a possible potential predictive factor of poor prognosis in OC patients.
As epidemiological studies have reported decreased incidence of ovarian cancer associated with regular intake of NSAIDs, we assessed whether NSAIDs could have chemoadjuvant applications in EOC and found that (i) NSAID Indomethacin induces robust cell death in primary patient-derived platinum-sensitive and platinum- resistant ovarian cancer cells and ovarian cancer stem cells and (ii) downregulation of β-catenin is partially driving effects of Indomethacin in cisplatin-resistant cells.
Taken together, this study showed that Annexin A2 inhibition suppresses proliferation and invasion in ovarian cancer via β-catenin/EMT, proposing the potential role of Annexin A2 in the prevention and treatment of ovarian cancer.
These results uncover β-catenin as a critical factor in promoting ovarian cancer aggressiveness and a new mechanism linking between β-catenin and miRNA downregulation underlying this process.
Our study identifies activated Wnt signalling to be a marker for precursor lesions of OC and successfully develops a mouse model that mimics the earliest events in pathogenesis of OC by constitutively activating βcatenin.