A Critical Review of a Primary Mcb Paper: a Wnt–Axin2–Gsk3Β Cascade Regulates Snail1 Activity in Breast Cancer Cells

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A critical review of a primary MCB paper: A Wnt–Axin2–GSK3β cascade regulates Snail1 activity in breast cancer cells

Hypothesis:

By compilation of available evidence, Yook et al state that through hyperactive Wnt signalling, β-catenin-T-Cell factor [TCF] triggers epithelial mesenchymal transition [EMT] in human breast cancer cells. They then hypothesise that canonical Wnt signalling can result in tumour cell dedifferentiation and tissue-invasive activity - through an Axin2-dependent pathway. They aim to demonstrate this can occur by the stabilisation of the zinc transcription factor, Snail1 that they state plays an imperative regulation role of EMT programmes.

Comment: The context of the experiment including present-day scientific evidence and present-day understanding was well established on the onset. However, the opening paragraph is a somewhat convoluted blend of the author’s experimental aims supported by an array of scientific facts. It’s hard to discern which of these were deduced prior-to and which post- their experimentation. A description of the experiments and hypotheses being tested: including the controls used, number of experimental replicates and the statistical analysis used. A critique of how effectively the data is presented. Finally, does the experimental data really show what the authors say it does?

Figure 1 is subdivided into four panels: 1a-1d – each visually recording results of experiments investigating particular questions that collectively challenged the hypothesis to test its validity.

Figure 1a shows the confocal microscopy results of mock-transfected fluorescently-labelled MCF-7 cells and Wnt expressing tumour MCF-7 cells cultured on the vascularised epithelial-stromal tissue of the chorioallantoic membrane [CAM] of 11-day-old chick embryos. The authors hypothesised the mock-transferred MCF-7 cells would remain confined to the upper CAM surface as they were unable to express a tissue-invasive phenotype as...
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