The potential of targeting Wnt/β-catenin in colon cancer

Sebio, Ana; Kahn, Michaël; Lenz, Heinz‐Josef

doi:10.1517/14728222.2014.906580

Cited by 204 publications

(156 citation statements)

References 16 publications

(15 reference statements)

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“…Wnt/β-catenin signaling is involved in the development of the central nervous system, reproductive tract, breast, kidney, limbs, placenta, hair and bone (25). The expression imbalance of Wnt/β-catenin pathway constituents may result in embryonic death or abnormal embryonic development (25).…”

Section: Discussionmentioning

confidence: 99%

EZH2 inhibition promotes methyl jasmonate‑induced apoptosis of human colorectal cancer through the Wnt/β‑catenin pathway

et al. 2018

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Abstract. Methyl jasmonate potentially induces the differentiation of human myeloid leukemia cells and inhibits their proliferation; it may induce the differentiation and apoptosis of human lymphocytic leukemia cells, but does not exert a damaging effect on normal lymphocytes. In the present study, the anticancer effect of methyl jasmonate on human colorectal cancer cells was investigated. Cell viability and apoptosis was assessed using a Cell Counting kit-8 assay and flow cytometry, respectively. Methyl jasmonate suppressed cell viability and induced apoptosis in human colorectal cancer cells. Additionally, methyl jasmonate increased the activation of caspase-3, inhibited the expression levels of enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) and the Wnt/β-catenin pathway in human colorectal cancer. Downregulation of EZH2 expression enhanced the anticancer effect of methyl jasmonate on human colorectal cancer cells through suppression of the Wnt/β-catenin pathway. Thus, EZH2 downregulation promotes the anticancer effect of methyl jasmonate by inducing apoptosis in human colorectal cancer cells through the Wnt/β-catenin pathway.

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Section: Discussionmentioning

confidence: 99%

EZH2 inhibition promotes methyl jasmonate‑induced apoptosis of human colorectal cancer through the Wnt/β‑catenin pathway

et al. 2018

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“…2) that prevents the interaction of Wnts with their primary receptors. One such recombinant protein, Ipafricept (OMP-54F28), has reached clinical trials (21,22). It is likely that Ipafricept may interact with a subset of the 19 Wnt ligands.…”

Section: Upstream Inhibitors Of Wnt Production and Functionmentioning

confidence: 99%

Targeting Wnts at the Source—New Mechanisms, New Biomarkers, New Drugs

Madan

Virshup

2015

Molecular Cancer Therapeutics

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Wnt signaling is dysregulated in many cancers and is therefore an attractive therapeutic target. The focus of drug development has recently shifted away from downstream inhibitors of b-catenin. Active inhibitors of Wnt secretion and Wnt/receptor interactions have been developed that are now entering clinical trials. Such agents include inhibitors of Wnt secretion, as well as recombinant proteins that minimize Wnt-Frizzled interactions. These new therapies arrive together with the recent insight that cancer-specific upregulation of Wnt receptors at the cell surface regulates cellular sensitivity to Wnts. Loss-of-function mutations in RNF43 or ZNRF3 and gain-of-function chromosome translocations involving RSPO2 and RSPO3 are surprisingly common and markedly increase Wnt/b-catenin signaling in response to secreted Wnts. These mutations may be predictive biomarkers to select patients responsive to newly developed upstream Wnt inhibitors.

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“…The wnt/β-catenin signaling pathway has critical roles in embryonic development and carcinogenesis (30)(31)(32)(33)(34). It has been demonstrated that the wnt/β-catenin signaling pathway regulates EMT in cancer (35)(36)(37).…”

Section: Primer Sequence (5'-3') ------------------------------------mentioning

confidence: 99%

The role of aplysia ras homolog I in colon cancer cell invasion and adhesion

Ouyang

Pan

2017

Exp Ther Med

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Abstract. Aplysia ras homolog I (ARHI) acts as a tumor suppressor in certain cancer cells. However, the role of ARHI in colon cancer development has not previously been reported. The present study aimed to investigate the functional role of ARHI in colon cancer focusing on the aspect of metastasis. Furthermore, the molecular mechanism underlying its function was explored. The present study detected the expression of ARHI in a human colon epithelial cell line and colon cancer cell lines using reverse transcription-quantitative polymerase chain reaction and western blotting analysis. It was demonstrated that ARHI expression was significantly downregulated in colon cancer cell lines compared with the normal colon epithelial cell line (P<0.05). An ARHI-pcDNA3.1 plasmid was transfected into HCT116 cells to overexpress ARHI. The number of invaded cells and the adhesive ability were significantly decreased in the ARHI overexpression group compared with the control group, as determined by cell invasion and adhesion assays (P<0.05). Furthermore, ARHI overexpression led to increased mRNA and protein expression levels of E-cadherin, and decreased mRNA and protein expression levels of N-cadherin and vimentin. Wnt/β-catenin signaling was suppressed in HCT116 cells overexpressing ARHI. Lithium chloride, a wnt/β-catenin signaling activator, was able to attenuate the effect of ARHI on HCT116 cell invasion and adhesion. In addition, the effect of ARHI on epithelial-mesenchymal transition (EMT) in HCT116 cells was reversed by the activation of wnt/β-catenin signaling. In conclusion, the present study provided novel evidence that ARHI could inhibit colon cancer cell invasion and adhesion through suppressing EMT, and these effects were achieved, at least partially, via the suppression of the wnt/β-catenin signaling pathway. The present findings may help in developing novel therapeutic approaches for colon cancer.

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The potential of targeting Wnt/β-catenin in colon cancer

Cited by 204 publications

References 16 publications

EZH2 inhibition promotes methyl jasmonate‑induced apoptosis of human colorectal cancer through the Wnt/β‑catenin pathway

EZH2 inhibition promotes methyl jasmonate‑induced apoptosis of human colorectal cancer through the Wnt/β‑catenin pathway

Targeting Wnts at the Source—New Mechanisms, New Biomarkers, New Drugs

The role of aplysia ras homolog I in colon cancer cell invasion and adhesion

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