Supplementary figures S2-S6. Supplementary Figure S2: A diagram depicting the location of the studied SNPs and miR-200a binding site in KEAP1 gene. Supplementary Figure S3: Association of KEAP1 rs11085735 with breast cancer survival among the KBCP and OBCS breast cancer cases. Supplementary Figure S4: Association of KEAP1 rs11085735 with breast cancer survival among the ER positive cases. Supplementary Figure S5: Association of KEAP1 rs11085735 with breast cancer survival among KBCP cases with lower (<1.33) KEAP1 protein expression. Supplementary Figure S6: Association of KEAP1 protein expression with breast cancer survival in univariate Kaplan-Meier analysis.

Supplementary Tables 1-9 from ST14 Gene Variant and Decreased Matriptase Protein Expression Predict Poor Breast Cancer Survival

Supplementary figures S1-5, materials and methods. 1) Supplementary figures and associated legends: - Figure S1. ERK silencing decreases breast cancer cell migration and invasion but does not influence cell proliferation. - Figure S2. ERK2 does not interact with actin or keratin 8 and ERK2 phosphorylation is supported by vimentin but not actin. - Figure S3. Fluorescence recovery of wild-type Slug-GFP after photobleaching (FRAP). - Figure S4. Mass spectrometric identification of ERK1/2-dependent phosphorylation sites on Slug and validation using a newly generated Slug phospho-serine-87 antibody. - Figure S5. The phosphorylation status of Slug does not influence repression of E-Cadherin, Slug nuclear localisation or stability. 2) Supplementary materials and methods 3) Supplementary references

Supplementary Figure 2B from ST14 Gene Variant and Decreased Matriptase Protein Expression Predict Poor Breast Cancer Survival

<p>PDF file - 73K, Predicted functional effects of the studied SNPs in NRF2 and SRXN1 genes</p>

<p>PDF file - 73K, Predicted functional effects of the studied SNPs in NRF2 and SRXN1 genes</p>

<p>PDF file - 68K, Association between NRF2 and SRXN1 protein expression</p>

Abstract Epithelial–mesenchymal transition (EMT) in cells is a developmental process adopted during tumorigenesis that promotes metastatic capacity. In this study, we advance understanding of EMT control in cancer cells with the description of a novel vimentin–ERK axis that regulates the transcriptional activity of Slug (SNAI2). Vimentin, ERK, and Slug exhibited overlapping subcellular localization in clinical specimens of triple-negative breast carcinoma. RNAi-mediated ablation of these gene products inhibited cancer cell migration and cell invasion through a laminin-rich matrix. Biochemical analyses demonstrated direct interaction of vimentin and ERK, which promoted ERK activation and enhanced vimentin transcription. Consistent with its role as an intermediate filament, vimentin acted as a scaffold to recruit Slug to ERK and promote Slug phosphorylation at serine-87. Site-directed mutagenesis established a requirement for ERK-mediated Slug phosphorylation in EMT initiation. Together, these findings identified a pivotal step in controlling the ability of Slug to organize hallmarks of EMT. Cancer Res; 75(11); 2349–62. ©2015 AACR.

PDF file - 40K, A diagram depicting the genetic location of the studied SNPs in the NRF2 and SRXN1 genes

Supplementary tables S1-S10. S1. Significant associations of the KEAP1 protein expression and receptor statuses; S2. Association of the KEAP1 protein expression with NRF2 protein expression; S3. Analyzed polymorphisms in the KEAP1 gene; S4. Significant associations of the KEAP1 SNP genotypes with KEAP1 protein expression; S5. Associations of the KEAP1 SNP s11085735 genotypes with NRF2 protein expression; S6. Associations of the KEAP1 SNPs with breast cancer survival in multivariate analysis among invasive KBCP and OBCS breast cancer cases separately; S7. Variables significantly associated with breast cancer survival in multivariate analysis among invasive KBCP and OBCS breast cancer cases; S8. Significant associations with breast cancer survival in univariate analysis (Kaplan-Meier) according to KEAP1 SNP rs11085735 genotypes among KBCP and OBCS ER positive cases, KBCP ER positive cases and KBCP cases with low/negative ({less than or equal to}1.33) KEAP1 protein expression levelS9. Variables significantly associated with breast cancer survival in multivariate analysis among ER positive KBCP breast cancer cases; S10. Variables significantly associated with breast cancer survival in multivariate analysis among (KBCP) cases with lower KEAP1 protein expression

Abstract The 19p13.1 breast cancer susceptibility locus is a modifier of breast cancer risk in BRCA1 mutation carriers and is also associated with the risk of ovarian cancer. Here, we investigated 19p13.1 variation and risk of breast cancer subtypes, defined by estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2) status, using 48,869 breast cancer cases and 49,787 controls from the Breast Cancer Association Consortium (BCAC). Variants from 19p13.1 were not associated with breast cancer overall or with ER-positive breast cancer but were significantly associated with ER-negative breast cancer risk [rs8170 OR, 1.10; 95% confidence interval (CI), 1.05–1.15; P = 3.49 × 10−5] and triple-negative (ER-, PR-, and HER2-negative) breast cancer (rs8170: OR, 1.22; 95% CI, 1.13–1.31; P = 2.22 × 10−7). However, rs8170 was no longer associated with ER-negative breast cancer risk when triple-negative cases were excluded (OR, 0.98; 95% CI, 0.89–1.07; P = 0.62). In addition, a combined analysis of triple-negative cases from BCAC and the Triple Negative Breast Cancer Consortium (TNBCC; N = 3,566) identified a genome-wide significant association between rs8170 and triple-negative breast cancer risk (OR, 1.25; 95% CI, 1.18–1.33; P = 3.31 × 10−13]. Thus, 19p13.1 is the first triple-negative–specific breast cancer risk locus and the first locus specific to a histologic subtype defined by ER, PR, and HER2 to be identified. These findings provide convincing evidence that genetic susceptibility to breast cancer varies by tumor subtype and that triple-negative tumors and other subtypes likely arise through distinct etiologic pathways. Cancer Res; 72(7); 1795–803. ©2012 AACR.

<p>PDF file - 43K, Clinicopathological characteristics of the patients</p>

Supplementary Figure S1. Immunohistochemical staining of KEAP1 in breast tumor tissue.

PDF file - 1.2MB, Survival curves for breast cancer survival according to NRF2 and SRXN1 genotypes and protein expression

PDF file - 69K, Analysed SNPs in the NRF2 and the SRXN1 genes

<p>PDF file - 43K, Clinicopathological characteristics of the patients</p>

Supplementary table and figure legends

In this review proteins associated with tight junctions (TJs) is described with an emphasis on prostate cancer. Overall tight junctional proteins do not seem to play a decisive role in prostate carcinoma pathogenesis. Of TJ proteins, expression of some claudins show an association with clinical behaviour of the tumors. Claudin 1 expression appears to be related to a better prognosis partly due to its involvement in EMT abrogation. Claudin 3 and 4 are highly expressed in prostate cancer and their expression is associated with aggressive behaviour. Inhibition of claudin 8 promotes prostate carcinoma invasion and spread but studies are few. CPE has been known to bind to especially claudins 3 and 4 and cause cell lysis. Several experiments with modified CPE have been made in prostate cancer cell lines. Regardless of this effective CPE based human treatment for prostate cancer have not yet been developed.