scholarly journals Treating triple negative breast cancer cells with erlotinib plus a select antioxidant overcomes drug resistance by targeting cancer cell heterogeneity

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Bin Bao ◽  
Cristina Mitrea ◽  
Priyanga Wijesinghe ◽  
Luca Marchetti ◽  
Emily Girsch ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Cell Heterogeneity

scholarly journals Extracellular vesicles from triple-negative breast cancer cells promote proliferation and drug resistance in non-tumorigenic breast cells

2018 ◽  
Vol 172 (3) ◽  
pp. 713-723 ◽  
Author(s):  
Patricia Midori Murobushi Ozawa ◽  
Faris Alkhilaiwi ◽  
Iglenir João Cavalli ◽  
Danielle Malheiros ◽  
Enilze Maria de Souza Fonseca Ribeiro ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Extracellular Vesicles ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Breast Cells

Annexin A2 and its downstream IL-6 and HB-EGF as secretory biomarkers in the differential diagnosis of Her-2 negative breast cancer

2016 ◽  
Vol 54 (4) ◽  
pp. 463-471 ◽  
Author(s):  
Praveenkumar Shetty ◽  
Vidya S Patil ◽  
Rajashekar Mohan ◽  
Leonard Clinton D’souza ◽  
Anil Bargale ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Critical Role ◽  
Autocrine Regulation ◽  
Her 2 ◽  
Positive Breast Cancer

Background AnnexinA2 (AnxA2) membrane deposition has a critical role in HB-EGF shedding as well as IL-6 secretion in breast cancer cells. This autocrine cycle has a major role in cancer cell proliferation, migration and metastasis. The objective of the study is to demonstrate annexinA2-mediated autocrine regulation via HB-EGF and IL-6 in Her-2 negative breast cancer progression. Methods Secretory annexinA2, HB-EGF and IL-6 were analysed in the peripheral blood sample of Her-2 negative ( n = 20) and positive breast cancer patients ( n = 16). Simultaneously, tissue expression was analysed by immunohistochemistry. The membrane deposition of these secretory ligands and their autocrine regulation was demonstrated using triple-negative breast cancer cell line model. Results Annexina2 and HB-EGF expression are inversely correlated with Her-2, whereas IL-6 expression is seen in both Her-2 negative and positive breast cancer cells. RNA interference studies and upregulation of annexinA2 proved that annexinA2 is the upstream of this autocrine pathway. Abundant soluble serum annexinA2 is secreted in Her-2 negative breast cancer (359.28 ± 63.73 ng/mL) compared with normal (286.10 ± 70.04 ng/mL, P < 0.01) and Her-2 positive cases (217.75 ± 60.59 ng/mL, P < 0.0001). In Her-2 negative cases, the HB-EGF concentrations (179.16 ± 118.81 pg/mL) were highly significant compared with normal (14.92 ± 17.33 pg/mL, P < 0.001). IL-6 concentrations were increased significantly in both the breast cancer phenotypes as compared with normal ( P < 0.001). Conclusion The specific expression pattern of annexinA2 and HB-EGF in triple-negative breast cancer tissues, increased secretion compared with normal cells, and their major role in the regulation of EGFR downstream signalling makes these molecules as a potential tissue and serum biomarker and an excellent therapeutic target in Her-2 negative breast cancer.

scholarly journals Correction to: New insights in gene expression alteration as effect of doxorubicin drug resistance in triple negative breast cancer cells

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Cristina Alexandra Ciocan-Cartita ◽  
Ancuta Jurj ◽  
Oana Zanoaga ◽  
Roxana Cojocneanu ◽  
Laura-Ancuta Pop ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Gene Expression Alteration

An amendment to this paper has been published and can be accessed via the original article.

Supramolecular magnetonanohybrids for multimodal targeted therapy of triple-negative breast cancer cells

2020 ◽  
Vol 8 (32) ◽  
pp. 7166-7188 ◽  
Author(s):  
Alexandra A. P. Mansur ◽  
Herman S. Mansur ◽  
Alice G. Leonel ◽  
Isadora C. Carvalho ◽  
Manuela C. G. Lage ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative

All-in-one nanosoldier on a targeted mission: killing the triple-negative breast cancer cell enemy.

scholarly journals Glucose-limiting conditions induce an invasive population of MDA-MB-231 breast cancer cells with increased connexin 43 expression and membrane localization

2021 ◽  
Vol 15 (2) ◽  
pp. 223-236
Author(s):  
Jennifer C. Jones ◽  
Amanda M. Miceli ◽  
Mary M. Chaudhry ◽  
Chloe S. Kaunitz ◽  
Mallika A. Jai ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Triple Negative Breast Cancer ◽  
Nutrient Availability ◽  
Connexin 43 ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Low Glucose

AbstractGap junctional intercellular communication (GJIC) is a homeostatic process mediated by membrane channels composed of a protein family known as connexins. Alterations to channel activity can modulate suppression or facilitation of cancer progression. These varying roles are influenced by the cancer cell genetic profile and the context-dependent mechanisms of a dynamic extracellular environment that encompasses fluctuations to nutrient availability. To better explore the effects of altered cellular metabolism on GJIC in breast cancer, we generated a derivative of the triple-negative breast cancer cell line MDA-MB-231 optimized for growth in low-glucose. Reduced availability of glucose is commonly encountered during tumor development and leads to metabolic reprogramming in cancer cells. MDA-MB-231 low-glucose adapted cells exhibited a larger size with improved cell–cell contact and upregulation of cadherin-11. Additionally, increased protein levels of connexin 43 and greater plasma membrane localization were observed with a corresponding improvement in GJIC activity compared to the parental cell line. Since GJIC has been shown to affect cellular invasion in multiple cancer cell types, we evaluated the invasive qualities of these cells using multiple three-dimensional Matrigel growth models. Results of these experiments demonstrated a significantly more invasive phenotype. Moreover, a decrease in invasion was noted when GJIC was inhibited. Our results indicate a potential response of triple-negative breast cancer cells to reduced glucose availability that results in changes to GJIC and invasiveness. Delineation of this relationship may help elucidate mechanisms by which altered cancer cell metabolism affects GJIC and how cancer cells respond to nutrient availability in this regard.

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