M. Hung

Publications974
h-index148
Citations76,568
Highly Influential Citations3,302
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Dual regulation of Snail by GSK-3β-mediated phosphorylation in control of epithelial–mesenchymal transition
TLDR
It is shown that GSK-3β binds to and phosphorylates Snail at two consensus motifs to dually regulate the function of this protein and together function as a molecular switch for many signalling pathways that lead to EMT.
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PTEN activation contributes to tumor inhibition by trastuzumab, and loss of PTEN predicts trastuzumab resistance in patients.
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Nuclear localization of EGF receptor and its potential new role as a transcription factor
TLDR
It is demonstrated that nuclear EGFR is strongly correlated with highly proliferating activities of tissues and associated with promoter region of cyclin D1 in vivo, suggesting that EGFR might function as a transcription factor to activate genes required for highly proliferationating activities.
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Requirement for neuregulin receptor erbB2 in neural and cardiac development
TLDR
The results demonstrate the importance of erbB2 in neural and cardiac development and find that mutant embryos die before Ell, probably as a result of dysfunctions associated with a lack of cardiac trabeculae.
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HER-2/neu induces p53 ubiquitination via Akt-mediated MDM2 phosphorylation
TLDR
This study indicates that blocking the Akt pathway mediated by HER-2/neu would increase the cytotoxic effect of DNA-damaging drugs in tumour cells with wild-type p53.
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Epidermal growth factor receptor cooperates with signal transducer and activator of transcription 3 to induce epithelial-mesenchymal transition in cancer cells via up-regulation of TWIST gene…
TLDR
It is shown that EGF induces EGFR-expressing cancer cells to undergo a transition from the epithelial to the spindle-like mesenchymal morphology and induce cancer cell EMT via STAT3-mediated TWIST gene expression.
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An integrative genomic and proteomic analysis of PIK3CA, PTEN, and AKT mutations in breast cancer.
TLDR
PI3K pathway aberrations likely play a distinct role in the pathogenesis of different breast cancer subtypes and the specific aberration present may have implications for the selection of PI3K-targeted therapies in hormone receptor-positive breast cancer.
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IkappaB kinase promotes tumorigenesis through inhibition of forkhead FOXO3a.
TLDR
Evidence is provided for the negative regulation of FOXO factors by IKK as a key mechanism for promoting cell growth and tumorigenesis by showing that IkappaB kinase physically interacts with, phosphorylates, and inhibits FOXO3a independent of Akt and causes proteolysis of FOXo3a via the Ub-dependent proteasome pathway.
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ERK promotes tumorigenesis by inhibiting FOXO3a via MDM2-mediated degradation
TLDR
This study elucidates a novel pathway in cell growth and tumorigenesis through negative regulation of FOXO3a by RAS–ERK and MDM2 and downregulates Forkhead box O 3a by directly interacting with and phosphorylating FOXO 3a at Ser 294, Ser 344 and Ser 425.
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Cytoplasmic localization of p21Cip1/WAF1 by Akt-induced phosphorylation in HER-2/neu-overexpressing cells
TLDR
It is shown that HER-2/neu-mediated cell growth requires the activation of Akt, which associates with p 21Cip1/WAF1 and phosphorylates it at threonine 145, resulting in cytoplasmic localization of p21Cip 1/Waf1.
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