Among triple-negative breast cancers, HER2(0) breast cancer shows a strong tendency to be basal-like compared with HER2(1+) breast cancer: preliminary results

Nakagawa, Misako; Bando, Yoshimi; Nagao, Taeko; Takai, Chikako; Ohnishi, Takamasa; Honda, Junko; Moriya, Takuya; Izumi, Kiyotaka; Takahashi, Masako; Tangoku, Akira; Sasa, Mitsunori

doi:10.1007/s12282-011-0265-6

Cited by 7 publications

(3 citation statements)

References 25 publications

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“…Compared with the non-anthracycline drugs, hER2-positive breast cancer is more sensitive to the treatment of anthracycline-containing drugs. however, recent clinical studies have shown that, in fact, the predictive value of the efficacy of anthracycline drugs on HER2-positive breast cancer may be affectd by the synergistic amplification of the TOP2A gene (19). The TOP2A gene is adjacent to the hER2 gene, located in the 21 site of the long arm of chromosome 17, which is expressed as amplification or deletion in breast cancer with HER2 gene amplification.…”

Section: Discussionmentioning

confidence: 99%

Suppression of PTEN/AKT signaling decreases the expression of TUBB3 and TOP2A with subsequent inhibition of cell growth and induction of apoptosis in human breast cancer MCF-7 cells via ATP and caspase-3 signaling pathways

et al. 2017

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The aim of the present study was to evaluate the effects of PTEN/AKT signaling on TUBB3 and TOP2A expression and on the subsequent cell growth of human breast cancer MCF-7 cells. We found that the disease-free survival (DFS) and overall survival (OS) of breast cancer patients with TUBB3‑positive tumors were lower than these rates in the patients with TUBB3-negative tumors. Meanwhile, DFS and OS of breast cancer patients with TOP2A-positive tumors were also lower than these rates in patients with TOP2A-negative tumors. Suppression of PTEN reduced the protein expression of TUBB3 and TOP2A in MCF-7 cells. Suppression of PTEN also reduced cell proliferation and induced apoptosis and caspase-3 activity in MCF-7 cells. Moreover, an increase in ATP also reduced TUBB3 and TOP2A protein expression, reduced cell proliferation and induced apoptosis and caspase-3 activity in the MCF-7 cells following suppression of PTEN. Suppression of phosphorylation-AKT (p-AKT) reduced the protein expression of TUBB3 and TOP2A in the MCF-7 cells. Suppression of p-AKT also reduced cell proliferation and induced apoptosis and caspase-3 activity in the MCF-7 cells. Then, ATP also reduced TUBB3 and TOP2A protein expression, reduced cell proliferation and induced apoptosis and caspase-3 activity in MCF-7 cells following suppression of p-AKT. These results suggest that PTEN/AKT signaling affects the expression of TUBB3 and TOP2A reducing cell growth and inducing apoptosis of human breast cancer MCF-7 cells through ATP and caspase-3 signaling pathways. TUBB3 and TOP2A may be promising prognostic markers for the efficacy of adjuvant cisplatin-based chemotherapy.

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Section: Discussionmentioning

confidence: 99%

Suppression of PTEN/AKT signaling decreases the expression of TUBB3 and TOP2A with subsequent inhibition of cell growth and induction of apoptosis in human breast cancer MCF-7 cells via ATP and caspase-3 signaling pathways

et al. 2017

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“…One major way of defining the type of breast cancer is whether or not it is endocrine receptor (estrogen or progesterone receptor)-positive, HER2-positive, triple-negative (not positive to receptors for estrogen, progesterone or HER2) or triple-positive (positive for estrogen receptors, progesterone receptors and HER2) (7,8). These classifications provide oncologists with valuable information about how the tumor acts and what type of treatments may work best.…”

Section: Introductionmentioning

confidence: 99%

Effect of sodium/iodide symporter (NIS)-mediated radioiodine therapy on estrogen receptor-negative breast cancer

Yao

Pan

et al. 2015

Oncology Reports

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Since the sodium/iodide symporter (NIS) stimulates the iodine uptake in normal lactating breast, our study aimed to study the effect of NIS-mediated radioiodide therapy on ER-negative breast cancers. A recombinant lentivirus plasmid encoding the human NIS (hNIS) gene and firefly luciferase (Fluc) was constructed. MDA-MB-231 cells were transfected with the recombinant lentivirus, and the hNIS gene expression was identified by western blot analysis and real-time PCR. Tissue-specific expression of the NIS gene was confirmed by immunohistochemical (IHC) staining. Functional NIS activity in the MDA-hNIS cells was confirmed by the uptake of 131I and cytotoxicity assays. The relative expression level of hNIS mRNA exhibited a 10-fold higher expression in the MDA-hNIS cells compared with the level in the control cells without the endogenous NIS gene. Abundant expression of hNIS protein was noted in the cell membrane compared to the cytoplasm which confirmed the efficient expression of the functional hNIS gene. Iodine uptake into the MDA-hNIS cells was rapid, reaching a maximum after 15 min, followed by a decline. Exposure of the MDA-hNIS cells with 131I resulted in a time-dependent reduction in colony formation compared with the survival of the control (MDA) cells. Our results confirmed that NIS overexpression enhances the sensitivity of ER-negative breast cancer cells to radioiodide therapy.

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“…In particular, according to the new St. Gallen consensus recommendations, Ki67 is one of the prognostic markers that is considered important to subclassify luminal A and luminal B, together with HER2 expression (12). The absence of ER, PR and HER2 is used to define the triple-negative subtype, which represents ~15% of breast tumours and is not a homogeneous entity (13)(14)(15). Thus, new prognostic and/or predictive factors may provide additional risk stratifications to better guide treatment decisions in these different subtypes of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

Differential expression of testin and survivin in breast cancer subtypes

et al. 2013

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Abstract. Testin (TES) is a putative tumour-suppressor gene downregulated in various types of cancers. Survivin is a nodal protein involved in multiple signalling pathways, tumour maintenance and inhibition of apoptosis. Previous studies indicate that TES and survivin can functionally interact and modulate cell death and proliferation in breast cancer cells. The aim of the present study was to investigate the expression and prognostic relevance of TES and survivin in breast cancer subtypes examining a large cohort of breast cancer patients. We determined the expression of TES and survivin by immunohistochemistry (IHC) in tissue samples from 242 breast cancer patients diagnosed between 1981 and 2009. The expression of these proteins was compared with clinical and pathological data. There was a significant association of nuclear survivin overexpression and TES downregulation with triple-negative tumours [P=0.009; univariate odds ratio (OR), 3.20; 95% CI, 1.34-7.66] (P=0.018; multivariate OR, 2.90; 95% CI, 1.20-6.97). A further significant correlation was observed between TES downregulation and the luminal B subtype (P=0.019, univariate OR: 2.90; 95% CI, 1.19-7.06) (P=0.032, multivariate OR, 2.67; 95% CI, 1.09-6.65), independent of survivin expression. Our results demonstrated a statistically significant association between TES downregulation and highly aggressive breast tumour subtypes, such as triplenegative and luminal B tumours, along with the prognostic relevance of nuclear expression of survivin. To our knowledge, this is the first demonstration of such an association.

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Among triple-negative breast cancers, HER2(0) breast cancer shows a strong tendency to be basal-like compared with HER2(1+) breast cancer: preliminary results

Abstract: In TNBC, HER2(0) breast cancer showed a strong tendency to include more of the basal-like phenotype compared with HER2(1+) breast cancer. The staining results indicated the possibility that HER2(0) breast cancer and HER2(1+) breast cancer have different characteristics.

Cited by 7 publications

References 25 publications

Suppression of PTEN/AKT signaling decreases the expression of TUBB3 and TOP2A with subsequent inhibition of cell growth and induction of apoptosis in human breast cancer MCF-7 cells via ATP and caspase-3 signaling pathways

Suppression of PTEN/AKT signaling decreases the expression of TUBB3 and TOP2A with subsequent inhibition of cell growth and induction of apoptosis in human breast cancer MCF-7 cells via ATP and caspase-3 signaling pathways

Effect of sodium/iodide symporter (NIS)-mediated radioiodine therapy on estrogen receptor-negative breast cancer

Differential expression of testin and survivin in breast cancer subtypes

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