Dataset Information

Expression of Tropomyosin 1 Gene Isoforms in Human Breast Cancer Cell Lines.

ABSTRACT: Nine malignant breast epithelial cell lines and 3 normal breast cell lines were examined for stress fiber formation and expression of TPM1 isoform-specific RNAs and proteins. Stress fiber formation was strong (++++) in the normal cell lines and varied among the malignant cell lines (negative to +++). Although TPM1? and TPM1? were the dominant transcripts of TPM1, there was no clear evidence for TPM1? protein expression. Four novel human TPM1 gene RNA isoforms were discovered (?, ?, ?, and ?), which were not identified in adult and fetal human cardiac tissues. TPM1? was the most frequent isoform expressed in the malignant breast cell lines, and it was absent in normal breast epithelial cell lines. By western blotting, we were unable to distinguish between TPM1?, ?, and ? protein expression, which were the only TPM1 gene protein isoforms potentially expressed. Some malignant cell lines demonstrated increased or decreased expression of these isoforms relative to the normal breast cell lines. Stress fiber formation did not correlate with TPM1? RNA expression but significantly and inversely correlated with TPM1? and TPM1? expression, respectively. The exact differences in expression of these novel isoforms and their functional properties in breast epithelial cells will require further study.

SUBMITTER: Dube S

PROVIDER: S-EPMC4480939 | biostudies-other | 2015

REPOSITORIES: biostudies-other

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Expression of Tropomyosin 1 Gene Isoforms in Human Breast Cancer Cell Lines.

Dube Syamalima S Yalamanchili Santhi S Lachant Joseph J Abbott Lynn L Benz Patricia P Mitschow Charles C Dube Dipak K DK Poiesz Bernard J BJ

International journal of breast cancer 20150611

Nine malignant breast epithelial cell lines and 3 normal breast cell lines were examined for stress fiber formation and expression of TPM1 isoform-specific RNAs and proteins. Stress fiber formation was strong (++++) in the normal cell lines and varied among the malignant cell lines (negative to +++). Although TPM1γ and TPM1δ were the dominant transcripts of TPM1, there was no clear evidence for TPM1δ protein expression. Four novel human TPM1 gene RNA isoforms were discovered (λ, μ, ν, and ξ), wh ...[more]

PMID: 26171250

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Project description:Recurrent mutations in histone modifying enzymes in multiple cancer types imply key roles in tumorigenesis. However, the functional relevance of these mutations remains unknown. Here we show that the JARID1B histone H3 lysine 4 demethylase is frequently amplified and overexpressed in luminal breast tumors and a somatic point mutation of JARID1B leads to the gain of luminal-specific gene expression programs. Downregulation of JARID1B in luminal breast cancer cells induces the expression of basal cell-specific genes and growth arrest, which is partially rescued by the inhibition of TGFBR thereby indicating a key role for TGFb signaling. Integrated genome-wide analysis of JARID1B chromatin binding, histone H3 lysine trimethyl (H3K4me3) and dimethyl (H3K4me2) patterns, and gene expression profiles in luminal and basal-like breast cancer cells suggest a key role for JARID1B in luminal cell-specific gene expression programs. A significant fraction of JARID1B binding-sites overlaps with CTCF in both luminal and basal-like breast cancer cells. CTCF also co-immunoprecipitates with JARID1B and it may influence its histone demethylase (HDM) activity as the H3K4me3/me2 ratio is lower at the CTCF-overlapping compared to JARID1B-unique sites. Additionally, a heterozygous JARID1B missense mutation (K1435R) in the HCC2157 basal-like breast cancer cell line is associated with unique JARID1B chromatin-binding and gene expression patterns implying gain of luminal features. In line with this, exogenous expression of this mutant in basal-like breast cancer cells leads to a gain of JARID1B binding at many luminal-specific genes. A PARADIGM score reflecting JARID1B activity in luminal breast cancer cells is associated with poor clinical outcome in patients with luminal breast tumors. Together, our data imply that JARID1B is a luminal lineage-driving oncogene and that its therapeutic targeting may represent a novel therapeutic strategy in treatment-resistant luminal breast tumors. RNA-Seq in breast cancer cell-lines transfected with JARID1B/CTCF/control siRNA. 50 cycles of sequencing on Illumina platform.

Dataset Information

Expression of Tropomyosin 1 Gene Isoforms in Human Breast Cancer Cell Lines.

Publications

Expression of Tropomyosin 1 Gene Isoforms in Human Breast Cancer Cell Lines.

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