scholarly journals The Predictive Role of E-cadherin and Androgen Receptor on In Vitro Chemosensitivity in Triple-negative Breast Cancer

2009 ◽  
Vol 39 (9) ◽  
pp. 560-568 ◽  
Author(s):  
J. S. Koo ◽  
W. Jung ◽  
J. Jeong
Keyword(s):  
Breast Cancer ◽  
Androgen Receptor ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
In Vitro Chemosensitivity ◽  
Predictive Role ◽  
E Cadherin

scholarly journals Antiproliferative Effect of Androgen Receptor Inhibition in Mesenchymal Stem-Like Triple-Negative Breast Cancer

2016 ◽  
Vol 38 (3) ◽  
pp. 1003-1014 ◽  
Author(s):  
Aiyu Zhu ◽  
Yan Li ◽  
Wei Song ◽  
Yumei Xu ◽  
Fang Yang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Androgen Receptor ◽  
Cyclin D1 ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative

Background/Aims: Androgen receptor (AR), a steroid hormone receptor, has recently emerged as prognostic and treatment-predictive marker in breast cancer. Previous studies have shown that AR is widely expressed in up to one-third of triple-negative breast cancer (TNBC). However, the role of AR in TNBC is still not fully understood, especially in mesenchymal stem-like (MSL) TNBC cells. Methods: MSL TNBC MDA-MB-231 and Hs578T breast cancer cells were exposed to various concentration of agonist 5-α-dihydrotestosterone (DHT) or nonsteroidal antagonist bicalutamide or untreated. The effects of AR on cell viability and apoptosis were determined by MTT assay, cell counting, flow cytometry analysis and protein expression of p53, p73, p21 and Cyclin D1 were analyzed by western blotting. The bindings of AR to p73 and p21 promoter were detected by ChIP assay. MDA-MB-231 cells were transplanted into nude mice and the tumor growth curves were determined and expression of AR, p73 and p21 were detected by Immunohistochemistry (IHC) staining after treatment of DHT or bicalutamide. Results: We demonstrate that AR agonist DHT induces MSL TNBC breast cancer cells proliferation and inhibits apoptosis in vitro. Similarly, activated AR significantly increases viability of MDA-MB-231 xenografts in vivo. On the contrary, AR antagonist, bicalutamide, causes apoptosis and exerts inhibitory effects on the growth of breast cancer. Moreover, DHT-dependent activation of AR involves regulation in the cell cycle related genes, including p73, p21 and Cyclin D1. Further investigations indicate the modulation of AR on p73 and p21 mediated by direct binding of AR to their promoters, and DHT could make these binding more effectively. Conclusions: Our study demonstrates the tumorigenesis role of AR and the inhibitory effect of bicalutamide in AR-positive MSL TNBC both in vitro and in vivo, suggesting that AR inhibition could be a potential therapeutic approach for AR-positive TNBC patients.

1893 The role of Androgen Receptor, E-cadherin and Ki67 as novel prognostic markers in Triple Negative Breast Cancer (TNBC)

2015 ◽  
Vol 51 ◽  
pp. S297 ◽  
Author(s):  
G. Ricciardi ◽  
B. Adamo ◽  
V. Barresi ◽  
A. Ieni ◽  
T. Franchina ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Androgen Receptor ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Prognostic Markers ◽  
E Cadherin

scholarly journals The predictive role of estrogen receptor beta (ER-β) in androgen receptor (AR)-positive triple-negative breast cancer (TNBC)

2018 ◽  
Vol 29 ◽  
pp. iii32
Author(s):  
A. Anestis ◽  
C. Mihailidou ◽  
S. Theocharis ◽  
D. Tryfonopoulos ◽  
A. Korogiannos ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Estrogen Receptor Beta ◽  
Predictive Role ◽  
Receptor Beta

Prognostic markers in triple-negative breast cancer (TNBC): The role of androgen receptor, e-cadherin, and Ki67.

2015 ◽  
Vol 33 (15_suppl) ◽  
pp. 1089-1089
Author(s):  
Giuseppina Rosaria Rita Ricciardi ◽  
Barbara Adamo ◽  
Valeria Barresi ◽  
Antonio Ieni ◽  
Tindara Franchina ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Androgen Receptor ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Prognostic Markers ◽  
E Cadherin

CTNND1 to mediate bone metastasis of triple-negative breast cancer via regulating CXCR4.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e13045-e13045
Author(s):  
Chang Gong ◽  
Qun Lin ◽  
Xiaolin Fang ◽  
Wenguo Jiang ◽  
Jun Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bone Metastasis ◽  
High Throughput ◽  
Triple Negative Breast Cancer ◽  
High Throughput Sequencing ◽  
Triple Negative ◽  
Mtor Pathway ◽  
Tissue Samples

e13045 Background: Compared to lumial breast cancer, the proporation of triple-negative breast cancer (TNBC) with bone metastases (BMs) is relatively low and few data focusing on the mechanism of the BMs in TNBC are available, Here, we screened that CTNND1 was associated with BMs of TNBC by integrating high-throughput sequencing, and further investigated the role of CTNND1 in BMs of TNBC in vitro. Methods: TNBC tissue samples with only BMs (n = 6) and without any metastasis (n = 10) were tested using high-throughput sequencing and 11 differentially expressed relative genes were identified. We then quantified these 11 genes in normal breast tissue samples (n = 26), TNBC tissue samples with only BMs (n = 10), TNBC tissue samples without any metastasis (n = 88) as well as luminal tissue samples with BMs（n = 10）through qPCR and immunohistochemical staining (IHC). The effects of knocking down CTNND1 on the interaction between TNBC cells and osteoblasts were examined by cell adhesion, transwell migration and matrigel invasion assays. To explorethe role of CTNND1 in mediating bone metastasis in TNBC, we used RNA-sequencing to find out the relative downstream gene CXCR4 and PI3K-AKT-mTOR pathway and verified it in vitro by Western Blotting. Results: Combining our high-throughput sequencing data, qPCR and IHC in clinical tissue samples, we verified that CTNND1 was decreased in TNBC patients with bone metastasis compared to normal tissue and luminal tissue with BMs. Knocking down of CTNND1 in TNBC cells including MDA-MB-231, MDA-MB-468 and BT549 weakened cells adhesion, but facilitated cells migration and invasion. Mechanically, knocking down of CTNND1 upregulated CXCR4 via activating PI3K-AKT-mTOR pathway in TNBC but not luminal and HER2- positive breast cancer cells lines. Conclusions: CTNND1 mediates bone metastasis in triple-negative breast cancer via regulating CXCR4.CTNND1 may serve as a potential predictor of bone metastasis for TNBC patients.

scholarly journals LncRNA PAPAS may promote triple-negative breast cancer by downregulating miR-34a

2019 ◽  
Vol 47 (8) ◽  
pp. 3709-3718 ◽  
Author(s):  
Yan Kong ◽  
Cuizhi Geng ◽  
Qian Dong
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Cancer Biology ◽  
Triple Negative ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Healthy Controls ◽  
Plasma Samples

Objective To investigate the role of promoter and pre-rRNA antisense (PAPAS) long noncoding (Lnc) RNA in cancer biology. Methods Tumour and tumour-adjacent healthy tissue biopsies from patients with triple-negative breast cancer (TNBC), and plasma samples from these patients plus healthy controls, were assessed for PAPAS and microRNA (miR)-34a. Effects of PAPAS and miR-34a overexpression were also investigated in vitro. Results PAPAS was upregulated in tumour tissues of patients with TNBC versus tumour-adjacent healthy tissues. Plasma PAPAS levels were also upregulated in patients with TNBC versus healthy controls. Levels of PAPAS in tumour tissue was significantly positively correlated with PAPAS levels in plasma from patients with TNBC. MiR-34a was downregulated in tumour tissues versus adjacent healthy tissues, and was significantly correlated with PAPAS in tumour tissues. PAPAS overexpression in vitro was associated with miR-34a inhibition, while miR-34a failed to significantly affect PAPAS levels. PAPAS overexpression promoted in vitro migration and invasion of TNBC cells, while miR-34a overexpression was inhibitory. MiR-34a overexpression decreased the enhanced cell migration and invasion associated with PAPAS overexpression. PAPAS overexpression showed no significant effects on cancer-cell proliferation. Conclusion LncRNA PAPAS may promote TNBC by downregulating miR-34a.

scholarly journals Prognostic Role of Androgen Receptor in Triple Negative Breast Cancer: A Multi-Institutional Study

Cancers ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 995 ◽  
Author(s):  
Shristi Bhattarai ◽  
Sergey Klimov ◽  
Karuna Mittal ◽  
Uma Krishnamurti ◽  
Xiaoxian Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Androgen Receptor ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Molecular Subtype ◽  
Good Prognosis ◽  
Prognostic Role ◽  
Primary Tumors ◽  
Total N

Background: The androgen receptor (AR) has emerged as a potential therapeutic target for AR-positive triple-negative breast cancer (TNBC). However, conflicting reports regarding AR’s prognostic role in TNBC are putting its usefulness in question. Some studies conclude that AR positivity indicates a good prognosis in TNBC, whereas others suggest the opposite, and some show that AR status has no significant bearing on the patients’ prognosis. Methods: We evaluated the prognostic value of AR in resected primary tumors from TNBC patients from six international cohorts {US (n = 420), UK (n = 239), Norway (n = 104), Ireland (n = 222), Nigeria (n = 180), and India (n = 242); total n = 1407}. All TNBC samples were stained with the same anti-AR antibody using the same immunohistochemistry protocol, and samples with ≥1% of AR-positive nuclei were deemed AR-positive TNBCs. Results: AR status shows population-specific patterns of association with patients’ overall survival after controlling for age, grade, population, and chemotherapy. We found AR-positive status to be a marker of good prognosis in US and Nigerian cohorts, a marker of poor prognosis in Norway, Ireland and Indian cohorts, and neutral in UK cohort. Conclusion: AR status, on its own, is not a reliable prognostic marker. More research to investigate molecular subtype composition among the different cohorts is warranted.

scholarly journals PROGNOSIS OF NEOADJUVANT CHEMOTHERAPY EFFICACY WITH IMMUNOBIOLOGIC TUMOR MARKERS IN PATIENTS WITH TRIPLE NEGATIVE BREAST CANCER

2019 ◽  
pp. 46-54
Author(s):  
S. A. Lyalkin ◽  
N. O. Verevkina ◽  
L. A. Syvak
Keyword(s):  
Breast Cancer ◽  
Neoadjuvant Chemotherapy ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Fold Increase ◽  
Predictive Role ◽  
High Level ◽  
Chemotherapy Efficacy ◽  
Cd4 Lymphocytes

Treatment of patients with triple negative breast cancer (TNBC) remains one of the most difficult problems in clinical oncology. Despite the negative prognosis for TNBC, there exists the group of patients with better response to the therapy and better prognosis, which proves the heterogenity of TNBC. The aim of the study was to evaluate the predictive role of tumor infiltrative lymphocytes (TIL) and their subpopulations (CD4+, CD8+ and FOXP3) in patients with TNBC. The predictive role of clinical, morphologic and immunohystochemical tumor features on neoadjuvant chemotherapy (NACT) efficacy was assessed in 52 TNBC patients. The risk of incomplete pathomorphologic response after NACT is related with 2 biomarkers: level of TIL and stromal CD4+ lymphocytes. The increase of TIL level decreases of the risk of incomplete pathomorphologic response (P = 0.01), ОR = 0.07 (95 % CІ 0.01–0.55) while standartization on CD4+ level. The high level of TIL at the time of diagnosis significantly decreases the risk of incomplete pathomorphologic response (OR = 0,2; P = 0,02). The group of patients with the ratio of stromal lymphocytes CD4low/CD8low had the eight-fold increase of the risk of incomplete pathomorphologic response comparing with the group with the ratio CD4high/CD8high (ОR = 8,0; Р = 0,03); the patient with the ratio stromal lymphocytes CD8low/ FOXP3low had the almost two-fold increase of the risk of incomplete pathomorphologic response comparing with the group with the ratio CD8high/FOXP3high (ОR = 2,1; Р = 0,03).

scholarly journals Lamin B2 promotes the progression of triple negative breast cancer via mediating cell proliferation and apoptosis

2021 ◽  
Vol 41 (1) ◽  
Author(s):  
Cui-Cui Zhao ◽  
Jing Chen ◽  
Li-Ying Zhang ◽  
Hong Liu ◽  
Chuan-Gui Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
The Cancer Genome Atlas ◽  
Proliferation And Apoptosis

Abstract Triple negative breast cancer (TNBC) is a more common type of breast cancer with high distant metastasis and poor prognosis. The potential role of lamins in cancer progression has been widely revealed. However, the function of lamin B2 (LMNB2) in TNBC progression is still unclear. The present study aimed to investigate the role of LMNB2 in TNBC. The cancer genome atlas (TCGA) database analysis and immunohistochemistry (IHC) were performed to examine LMNB2 expression levels. LMNB2 short hairpin RNA plasmid or lentivirus was used to deplete the expression of LMNB2 in human TNBC cell lines including MDA-MB-468 and MDA-MB-231. Alterations in cell proliferation and apoptosis in vitro and the nude mouse tumorigenicity assay in vivo were subsequently analyzed. The human TNBC tissues shown high expression of LMNB2 according to the bioinformation analysis and IHC assays. LMNB2 expression was correlated with the clinical pathological features of TNBC patients, including pTNM stage and lymph node metastasis. Through in vitro and in vivo assays, we confirmed LMNB2 depletion suppressed the proliferation and induced the apoptosis of TNBC cells, and inhibited tumor growth of TNBC cells in mice, with the decrease in Ki67 expression or the increase in caspase-3 expression. In conclusion, LMNB2 may promote TNBC progression and could serve as a potential therapeutic target for TNBC treatment.

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