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CapG a putative oncogen affects gene expression in breast cancer cells

ABSTRACT: The transition from ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) is an important step during breast tumorgenesis. Understanding its molecular changes may uncover both novel preventive and therapeutic strategies and may help to identify high-risk DCIS that progress to IDC. The mechanisms are unknown and the role of CapG in the nucleus is an enigma. Here, we tested the association between clinicopathological CapG expression in tumor samples and used a cell culture model to test the hypothesis that CapG affects gene expression. Breast cancer samples were analyzed by reverse transcriptase – real time PCR (RT-qPCR). We used microarray analysis to study the transcriptome of the cell culture model and validated changes in gene expression in laser capture micro-dissected formalin-fixed paraffin-embedded (FFPE) invasive ductal carcinoma (IDC) and ductal carcinoma in situ (DCIS), respectively. We were able to associate increased CapG expression with an invasive breast cancer phenotype. In 28.2% of breast cancer samples CapG expression in breast cancer samples revealed in 28.2% a very high CapG expression and statistical significant association (p<0.05) to positive metastasis status (M1) and negative ER status (ER-). In case of CapG overexpression microarray analyses generated a list of differential expressed genes and revealed enhanced expression levels of GPNMB, NRP1, LOXL2, TRIM47 and COL16A1, while ZDHHC11, KIAA1467 were down-regulated. We show here for the first time an effect on the transcriptome by experimental modification of CapG expression. Concluding, CapG is involved in tumor progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53566 | GEO | 2017/11/30

SECONDARY ACCESSION(S): PRJNA232386

REPOSITORIES: GEO

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Project description:Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer where cells restricted to the ducts exhibit an atypical phenotype. Some DCIS lesions are believed to rapidly transit to invasive ductal carcinomas (IDCs), while others remain unchanged. Existing classification systems for DCIS fail to identify those lesions that transit to IDC. We studied gene expression patterns of 31 pure DCIS, 36 pure invasive cancers and 42 cases of mixed diagnosis (invasive cancer with an in situ component) using Agilent Whole Human Genome Oligo Microarrays 44k. Six normal breast tissue samples were also included as controls. qRT-PCR was used for validation. All DCIS and invasive samples could be classified into the intrinsic molecular subtypes defined for invasive breast cancer. Hierarchical clustering establishes that samples group by intrinsic subtype, and not by diagnosis. We observed heterogeneity in the transcriptomes among DCIS of high histological grade and identified a distinct subgroup containing seven of the 31 DCIS samples with gene expression characteristics more similar to advanced tumours. A set of genes independent of grade, ER-status and HER2-status was identified by logistic regression that univariately classified a sample as belonging to this distinct DCIS subgroup. qRT-PCR of single markers clearly separated this DCIS subgroup from the other DCIS, and contains samples from several histopathological and intrinsic molecular subtypes. The genes that differentiate between these two types of DCIS suggest several processes related to the re-organisation of the microenvironment. This raises interesting possibilities for identification of DCIS lesions both with and without invasive characteristics, which potentially could be used in clinical assessment of a woman's risk of progression, and lead to improved management that would avoid the current over- and under-treatment of patients. Breast cancer samples, 31 pure DCIS patients, 36 IDC patients, 42 mixed and 6 normal.

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CapG a putative oncogen affects gene expression in breast cancer cells

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