General strategy to analyse melanoma in mice

Gallagher, Stuart J.; Luciani, Flavie; Berlin, Irina; Rambow, Florian; Gros, Gwendoline; Champeval, Delphine; Delmas, Véronique; Larue, Lionel

doi:10.1111/j.1755-148x.2011.00907.x

Cited by 12 publications

(10 citation statements)

References 8 publications

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“…Whole-cell lysate was prepared from human melanoma cell lines using RIPA buffer and whole-tissue lysate was prepared from mouse melanoma tumour using SDS lysis buffer 53 . Membranes were probed with antibodies against ERK (Cell Signaling, 9102), pERK (Thr202/Thr204, Cell Signaling, 9106), CREB (Cell Signaling, 9192), pCREB (Cell Signaling, 9191S), PTEN (Cell Signaling, 9559), AKT (Cell Signaling, 2938), pAKT (Ser473, Cell Signaling 3787), GSK3-β (Santa-Cruz, sc-9166), pGSK3-β (Ser9, Cell Signaling, 9336), S6 (Cell Signaling, 2317), pS6 (Ser235/236) (Cell Signaling, 4857), β-catenin (Abcam, ab-6302), pβ-catenin (Ser675, Cell Signaling, 4176), pβ-catenin (Ser33-37/Thr41, Cell Signaling, 9561), pβ-catenin (Thr41/Ser45, Cell Signaling, 9565S), p16 (Santa-Cruz, sc-1661), CAV1 (Cell Signaling, 3238) and β-actin (Sigma, A5441).…”

Section: Methodsmentioning

confidence: 99%

A caveolin-dependent and PI3K/AKT-independent role of PTEN in β-catenin transcriptional activity

et al. 2015

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Loss of the tumour suppressor PTEN is frequent in human melanoma, results in MAPK activation, suppresses senescence and mediates metastatic behaviour. How PTEN loss mediates these effects is unknown. Here we show that loss of PTEN in epithelial and melanocytic cell lines induces the nuclear localization and transcriptional activation of β-catenin independent of the PI3K–AKT–GSK3β axis. The absence of PTEN leads to caveolin-1 (CAV1)-dependent β-catenin transcriptional modulation in vitro, cooperates with NRASQ61K to initiate melanomagenesis in vivo and induces efficient metastasis formation associated with E-cadherin internalization. The CAV1-β–catenin axis is mediated by a feedback loop in which β-catenin represses transcription of miR-199a-5p and miR-203, which suppress the levels of CAV1 mRNA in melanoma cells. These data reveal a mechanism by which loss of PTEN increases CAV1-mediated dissociation of β-catenin from membranous E-cadherin, which may promote senescence bypass and metastasis.

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Section: Methodsmentioning

confidence: 99%

A caveolin-dependent and PI3K/AKT-independent role of PTEN in β-catenin transcriptional activity

et al. 2015

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“…Tail-vein injection experiments and peritoneal metastasis assays were performed on nu/nu mice obtained as described elsewhere [ 22 ]. The 30 mice were divided into three groups randomly, namely ANXA2 high expression, ANXA2 low expression and mock groups.…”

Section: Methodsmentioning

confidence: 99%

Human epididymis protein 4 in association with Annexin II promotes invasion and metastasis of ovarian cancer cells

et al. 2014

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BackgroundThe objective of the present study was to identify human epididymis protein 4 (HE4) interacting proteins and explore the mechanisms underlying their effect on ovarian cancer cell invasion and metastasis.MethodsHE4 interacting proteins were identified by mass spectrometry and validated by co-immunoprecipitation and pull-down assays. The scratch test, the Transwell assay and animal experiments were used to assess the invasive and metastatic abilities of ovarian cancer cells before and after transfection and HE4 protein treatment. HE4 and annexin II protein expression in epithelial ovarian tissues was detected by immunohistochemistry, and the relation between their expression levels was examined.ResultsAnnexin II was identified as an HE4 interacting protein. HE4 and annexin II binding interaction promoted ovarian cancer cell invasion and metastasis. HE4 and annexin II expression levels were significantly higher in malignant epithelial ovarian tissues than in benign and normal epithelial ovarian tissues, and they were higher in tissues with lymph node metastases than in those without. HE4 gene interference downregulated the expression of MAPK and the FOCAL adhesion signaling pathway-associated molecules MKNK2 and LAMB2, and HE4 protein supplementation reversed this effect.ConclusionThe binding interaction between HE4 and annexin II activates the MAPK and FOCAL adhesion signaling pathways, promoting ovarian cancer cell invasion and metastasis.Electronic supplementary materialThe online version of this article (doi:10.1186/1476-4598-13-243) contains supplementary material, which is available to authorized users.

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“…Tail-vein injection experiments were performed on nu/nu mice obtained as described elsewhere (30). Small pieces (8 mm 3 ) of primary tumours from Nras or (Nras;bcat*) mice were initially implanted subcutaneously into the neck-pad of a nu/nu mouse.…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA was extracted and real-time RT-PCR carried out as previously described (30). The primer sequences are given in Sup.…”

Section: Methodsmentioning

confidence: 99%

Beta-catenin inhibits melanocyte migration but induces melanoma metastasis

et al. 2012

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The canonical Wnt signalling pathway induces the β-catenin/LEF transcription factors. It is activated in various cancers, most characteristically carcinomas, in which it promotes metastatic spread by increasing migration and/or invasion. The Wnt/β-catenin signalling pathway is frequently activated in melanoma, but the presence of β-catenin in the nucleus does not seem to be a sign of aggressiveness in these tumours. We found that, unlike its positive role in stimulating migration and invasion of carcinoma cells, β-catenin signalling decreased the migration of melanocytes and melanoma cell lines. In vivo, β-catenin signalling in melanoblasts reduced the migration of these cells, causing a white belly-spot phenotype. The inhibition, by β-catenin of migration was dependent on MITF-M, a key transcription factor of the melanocyte lineage, and CSK, a Src-inhibitor. Despite reducing migration, β-catenin signalling promoted lung metastasis in the Nras-driven melanoma murine model. Thus, β-catenin may play conflicting roles in the metastatic spread of melanoma, repressing migration while promoting metastasis. These results highlight that metastasis formation requires a series of successful cellular processes, any one of which may not be optimally efficient.

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General strategy to analyse melanoma in mice

Cited by 12 publications

References 8 publications

A caveolin-dependent and PI3K/AKT-independent role of PTEN in β-catenin transcriptional activity

A caveolin-dependent and PI3K/AKT-independent role of PTEN in β-catenin transcriptional activity

Human epididymis protein 4 in association with Annexin II promotes invasion and metastasis of ovarian cancer cells

Beta-catenin inhibits melanocyte migration but induces melanoma metastasis

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