Bmi-1, c-myc, and Snail expression in primary breast cancers and their metastases—elevated Bmi-1 expression in late breast cancer relapses

Joensuu, Kristiina; Hagström, Jaana; Leidenius, Marjut; Haglund, Caj; Andersson, Leif C.; Sariola, Hannu; Heikkilä, Päivi

doi:10.1007/s00428-011-1096-8

Cited by 29 publications

(23 citation statements)

References 44 publications

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“…protein overexpression in the epithelial component of breast cancer (6)(7)(8)(9)(22)(23)(24). However, we were unable to identify any correlation between MYC expression and axillary lymph node positivity in our series, confirming the results of previous studies (5,6,25).…”

Section: Clinicoc-myc (Cyt) C-myc (Nuc) Ki67 P-mtor P-akt Pathologicasupporting

confidence: 89%

“…Since lymph node status is an important factor in breast cancer staging and therapeutic options, the MYC status in compromised lymph nodes may represent a potential decision-making variable. MYC amplification and immunohistochemical staining were reported as being independent predictors of lymph node metastasis, but other studies did not report such a correlation (5)(6)(7).…”

Section: Introductionmentioning

confidence: 96%

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MYC is expressed in the stromal and epithelial cells of primary breast carcinoma and paired nodal metastases

Mundim

Pasini

Brentani

et al. 2015

Molecular and Clinical Oncology

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Abstract. The MYC oncogene is directly involved in the proliferation, metabolism, progression and distant metastasis of breast cancer. Since metastatic spread to the lymph nodes is often the first indication of propensity for metastatic dissemination, the MYC status in nodal disease may represent a decision-making variable. However, the analysis of MYC expression in stromal cells, namely cancer-associated fibroblasts (CAFs), which are known to play a critical role in cancer progression, remains poorly reported. The aim of this study was to determine the expression of MYC and other markers, including estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), p53, Ki67, epidermal growth factor receptor (EGFR), phosphorylated AKT (p-AKT) and phospho-mammalian target of rapamycin (p-mTOR) by immunohistochemistry in representative samples from 80 patients with ductal infiltrative breast cancer and 43 paired compromised axillary lymph nodes allocated in tissue microarrays (TMAs). The epithelial and stromal components of primary tumors and respective lymph node metastases were separately analyzed. MYC expression (cytoplasmic and nuclear) was a frequent event in the epithelial and stromal components of the primary tumors. The epithelial cells in the nodal metastases exhibited a trend for decreased MYC expression compared to that in the primary tumors (P=0.08) but retained the original status of the primary tumors for all other markers. The stromal cells were uniformly negative for ER, PR, HER2, p53, Ki67 and EGFR. Comparison of the stromas of primary tumors and respective lymph node metastases revealed a reduced frequency of nuclear MYC in 15% of the cases (P=0.003), whereas p-mTOR followed a similar trend (P=0.09). Analyses of the possible correlations among markers revealed that epithelial nuclear MYC was associated with p53 (P=0.048). This is an original study demonstrating a significant proportion of MYC expression (nuclear or cytoplasmic), as well p-mTOR and p-AKT expression, in the epithelial and stromal components of either the primary tumor or the nodal metastases. CAFs expressing MYC may establish an angiogenic microenvironment supporting cancer survival and facilitating colonization at the nodal metastatic site.

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Section: Clinicoc-myc (Cyt) C-myc (Nuc) Ki67 P-mtor P-akt Pathologicasupporting

confidence: 89%

Section: Introductionmentioning

confidence: 96%

MYC is expressed in the stromal and epithelial cells of primary breast carcinoma and paired nodal metastases

Mundim

Pasini

Brentani

et al. 2015

Molecular and Clinical Oncology

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“…By reviewing the full-text of the remaining 56 articles, 14 studies were finally included in our meta-analysis and were distributed into 5 studies (29.40%) with 789 cases (20%) for TWIST11319202122, 8 studies (47.06%) with 2,512 cases (63.69%) for SNAIL119212324252627, 2 studies (11.77%) with 89 cases (2.27%) for ZEB12128, and 2 studies (11.77%) with 551 cases (14.04%) for SLUG2930.…”

Section: Resultsmentioning

confidence: 99%

Prognostic Value of EMT-inducing Transcription Factors (EMT-TFs) in Metastatic Breast Cancer: A Systematic Review and Meta-analysis

Imani

Hosseinifard

Cheng

et al. 2016

Sci Rep

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The epithelial-to-mesenchymal transition (EMT) is a vital control point in metastatic breast cancer (MBC). TWIST1, SNAIL1, SLUG, and ZEB1, as key EMT-inducing transcription factors (EMT-TFs), are involved in MBC through different signaling cascades. This updated meta-analysis was conducted to assess the correlation between the expression of EMT-TFs and prognostic value in MBC patients. A total of 3,218 MBC patients from fourteen eligible studies were evaluated. The pooled hazard ratios (HR) for EMT-TFs suggested that high EMT-TF expression was significantly associated with poor prognosis in MBC patients (HRs = 1.72; 95% confidence intervals (CIs) = 1.53–1.93; P = 0.001). In addition, the overexpression of SLUG was the most impactful on the risk of MBC compared with TWIST1 and SNAIL1, which sponsored fixed models. Strikingly, the increased risk of MBC was less associated with ZEB1 expression. However, the EMT-TF expression levels significantly increased the risk of MBC in the Asian population (HR = 2.11, 95% CI = 1.70–2.62) without any publication bias (t = 1.70, P = 0.11). These findings suggest that the overexpression of potentially TWIST1, SNAIL1 and especially SLUG play a key role in the aggregation of MBC treatment as well as in the improvement of follow-up plans in Asian MBC patients.

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“…Overexpression of the c-myc gene has been found to be associated to the carcinogenesis, development and bad prognosis in a variety of tumors (He et al, 1995;Komiya et al, 2010;Joensuu et al, 2011). Moreover, previous reports have shown c-myc gene was amplification and overexpression in esophageal cancer cell lines (Jones et al, 1993;Kanda et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Luteolin Induced-growth Inhibition and Apoptosis of Human Esophageal Squamous Carcinoma Cell Line Eca109 Cells in vitro

Wang¹,

Wang²,

Huang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Luteolin is a plant flavonoid which exhibits anti-oxidative, anti-inflammatory and anti-tumor effects. However, the antiproliferative potential of luteolin is not fully understood. In this study, we investigated the effect of luteolin on cell cycling and apoptosis in human esophageal squamous carcinoma cell line Eca109 cells. MTT assays showed that luteolin had obvious cytotoxicity on Eca109 with an IC 50 of 70.7±1.72μM at 24h. Luteolin arrested cell cycle progression in the G0/G1 phase and prevented entry into S phase in a dose-and time-dependent manner. as assessed by FCM. Luteolin induced apoptosis of Eca109 cells was demonstrated by AO/EB staining assay and annexin V-FITC/PI staining. Moreover, luteolin downregulated the expression of cyclin D1, survivin and c-myc, and it also upregulated the expression of p53, in line with the fact that luteolin was able to inhibit Eca109 cell proliferation.

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Bmi-1, c-myc, and Snail expression in primary breast cancers and their metastases—elevated Bmi-1 expression in late breast cancer relapses

Cited by 29 publications

References 44 publications

MYC is expressed in the stromal and epithelial cells of primary breast carcinoma and paired nodal metastases

MYC is expressed in the stromal and epithelial cells of primary breast carcinoma and paired nodal metastases

Prognostic Value of EMT-inducing Transcription Factors (EMT-TFs) in Metastatic Breast Cancer: A Systematic Review and Meta-analysis

Luteolin Induced-growth Inhibition and Apoptosis of Human Esophageal Squamous Carcinoma Cell Line Eca109 Cells in vitro

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