Supplementary Table, Materials and References from Activity of dasatinib against L576P KIT mutant melanoma: Molecular, cellular, and clinical correlates

Epithelial-to-mesenchymal transition (EMT) is known to be important in regulating the behaviour of cancer cells enabling them to acquire stem cell characteristics or by enhancing the stem cell characteristics of cancer stem cells, resulting in these cells becoming more migratory and invasive. EMT can be driven by a number of mechanisms, including the TGF-β1 signalling pathway and/or by hypoxia. However, these drivers of EMT differ in their actions in regulating side population (SP) cell behaviour, even within SPs isolated from the same tissue. In this study we examined CoCl2 exposure and TGF-β driven EMT on SP cells of the MDA-MB-231 and MCF7 breast cancer cell lines. Both TGF-β1 and CoCl2 treatment led to the depletion of MDA-MB-231 SP. Whilst TGF-β1 treatment significantly reduced the MCF7 SP cells, CoCl2 exposure led to a significant increase. Single cell analysis revealed that CoCl2 exposure of MCF7 SP leads to increased expression of ABCG2 and HES1, both associated with multi-drug resistance. We also examined the mammosphere forming efficiency in response to CoCl2 exposure in these cell lines, and saw the same effect as seen with the SP cells. We suggest that these contrasting effects are due to ERα expression and the inversely correlated expression of TGFB-RII, which is almost absent in the MCF7 cells. Understanding the EMT-mediated mechanisms of the regulation of SP cells could enable the identification of new therapeutic targets in breast cancer.

mp3 file (7.5 MB). In the July edition of the Cancer Discovery podcast, Executive Editor Judy Quong talks with Lydia W.T. Cheung about her paper on the characterization of genetic mutations found in endometrial cancer.

Supplemental Tables 1, 2, 3

Supplementary Data from Integrative Analysis of Cyclin Protein Levels Identifies Cyclin B1 as a Classifier and Predictor of Outcomes in Breast Cancer

Supplementary Table Legends 1-3 from An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer

Supplementary Tables 1-3 from High Frequency of PIK3R1 and PIK3R2 Mutations in Endometrial Cancer Elucidates a Novel Mechanism for Regulation of PTEN Protein Stability

Supplementary figure 1. Genetic alterations in the PIK3CA, PTEN, AKT, MTOR, and HRAS genes from 279 HNSCC tumors from the TCGA.

Supplementary Materials and Methods from High Frequency of PIK3R1 and PIK3R2 Mutations in Endometrial Cancer Elucidates a Novel Mechanism for Regulation of PTEN Protein Stability

Supplementary Tables 5-8 from Characterization of a Naturally Occurring Breast Cancer Subset Enriched in Epithelial-to-Mesenchymal Transition and Stem Cell Characteristics

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Supplementary figure 3. Correlation of PI3K mutation, amplification, PI3K score, and mTOR score with sensitivity to GDC0941

Supplementary Legends for Figures and Tables 1-8 from Characterization of a Naturally Occurring Breast Cancer Subset Enriched in Epithelial-to-Mesenchymal Transition and Stem Cell Characteristics

Supplementary Tables 1-3 from Characterization of a Naturally Occurring Breast Cancer Subset Enriched in Epithelial-to-Mesenchymal Transition and Stem Cell Characteristics

Supplementary figure 2. Representative FISH data

Supplementary figure 5. MEK162 and GDC0941 effect on cell cycle

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Supplementary Table 4. STR profiles for cell lines used in this study.

Supplementary Data from Integrated Molecular and Clinical Analysis of AKT Activation in Metastatic Melanoma