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NFIB is a potential target for estrogen receptor-negative breast cancers.

ABSTRACT: The association between nuclear factor I/B (NFIB) gene and triple negative breast cancer has been previously suggested.We investigated the relationship between NFIB mRNA and protein expression and molecular subtypes of breast cancer as well as the effect of NFIB silencing on the proliferation and apoptosis of breast cancer cells. Also, the clinical importance of NFIB expression was investigated in 163 breast cancer patients.By using 20 frozen human breast cancer tissues and various breast cancer cell lines, we observed a significant high level of NFIB mRNA level in triple negative breast cancer. NFIB protein was upregulated in ER negative breast cancer tissues but the expression level was similar between HER2 subtype and triple negative subtype. The clinical significance of NFIB was further examined in a tissue microarray from 163 invasive breast cancer patients, and the immunohistochemistry results showed a significant association between NFIB expression and nuclear grade, ER, and HER2 expression status. NFIB positive tumors were more likely to have high nuclear grade, ER negativity and HER2 over-expression. HCC1954 cells transfected with siRNA against NFIB showed a significant reduction in cell proliferation and increase in apoptotic signaling pathway.Our results show a potential role of NFIB as a novel target in ER negative breast cancers.

SUBMITTER: Moon HG

PROVIDER: S-EPMC5528324 | biostudies-other | 2011 Dec

REPOSITORIES: biostudies-other

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Project description:BackgroundDirectly comparing gene expression profiles of estrogen receptor-positive (ER+) and estrogen receptor-negative (ER-) breast cancers cannot determine whether differentially expressed genes between these two subtypes result from dysregulated expression in ER+ cancer or ER- cancer versus normal controls, and thus would miss critical information for elucidating the transcriptomic difference between the two subtypes.Principal findingsUsing microarray datasets from TCGA, we classified the genes dysregulated in both ER+ and ER- cancers versus normal controls into two classes: (i) genes dysregulated in the same direction but to a different extent, and (ii) genes dysregulated to opposite directions, and then validated the two classes in RNA-sequencing datasets of independent cohorts. We showed that the genes dysregulated to a larger extent in ER+ cancers than in ER- cancers enriched in glycerophospholipid and polysaccharide metabolic processes, while the genes dysregulated to a larger extent in ER- cancers than in ER+ cancers enriched in cell proliferation. Phosphorylase kinase and enzymes of glycosylphosphatidylinositol (GPI) anchor biosynthesis were upregulated to a larger extent in ER+ cancers than in ER- cancers, whereas glycogen synthase and phospholipase A2 were downregulated to a larger extent in ER+ cancers than in ER- cancers. We also found that the genes oppositely dysregulated in the two subtypes significantly enriched with known cancer genes and tended to closely collaborate with the cancer genes. Furthermore, we showed the possibility that these oppositely dysregulated genes could contribute to carcinogenesis of ER+ and ER- cancers through rewiring different subpathways.ConclusionsGPI-anchor biosynthesis and glycogenolysis were elevated and hydrolysis of phospholipids was depleted to a larger extent in ER+ cancers than in ER- cancers. Our findings indicate that the genes oppositely dysregulated in the two subtypes are potential cancer genes which could contribute to carcinogenesis of both ER+ and ER- cancers through rewiring different subpathways.

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NFIB is a potential target for estrogen receptor-negative breast cancers.

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