scholarly journals In vitro and in vivo analysis of B-Myb in basal-like breast cancer

Oncogene ◽  
2008 ◽  
Vol 28 (5) ◽  
pp. 742-751 ◽  
Author(s):  
A R Thorner ◽  
K A Hoadley ◽  
J S Parker ◽  
S Winkel ◽  
R C Millikan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Basal Like Breast Cancer ◽  
In Vivo Analysis

scholarly journals Structure Based Design and Synthesis of Peptide Inhibitor of Human LOX-12: In Vitro and In Vivo Analysis of a Novel Therapeutic Agent for Breast Cancer

PLoS ONE ◽  
2012 ◽  
Vol 7 (2) ◽  
pp. e32521 ◽  
Author(s):  
Abhay kumar Singh ◽  
Ratnakar Singh ◽  
Farhat Naz ◽  
Shyam Singh Chauhan ◽  
Amit Dinda ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Therapeutic Agent ◽  
Peptide Inhibitor ◽  
Design And Synthesis ◽  
In Vivo Analysis ◽  
Novel Therapeutic

scholarly journals miR-146 connects stem cell identity with metabolism and pharmacological resistance in breast cancer

2021 ◽  
Vol 220 (5) ◽  
Author(s):  
Chiara Tordonato ◽  
Matteo Jacopo Marzi ◽  
Giovanni Giangreco ◽  
Stefano Freddi ◽  
Paola Bonetti ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Subtype ◽  
Transcriptional Analysis ◽  
Quiescent State ◽  
Tumor Initiating Cells ◽  
Physiological Relevance ◽  
Basal Like Breast Cancer ◽  
Xenograft Tumor Growth

Although ectopic overexpression of miRNAs can influence mammary normal and cancer stem cells (SCs/CSCs), their physiological relevance remains uncertain. Here, we show that miR-146 is relevant for SC/CSC activity. MiR-146a/b expression is high in SCs/CSCs from human/mouse primary mammary tissues, correlates with the basal-like breast cancer subtype, which typically has a high CSC content, and specifically distinguishes cells with SC/CSC identity. Loss of miR-146 reduces SC/CSC self-renewal in vitro and compromises patient-derived xenograft tumor growth in vivo, decreasing the number of tumor-initiating cells, thus supporting its pro-oncogenic function. Transcriptional analysis in mammary SC-like cells revealed that miR-146 has pleiotropic effects, reducing adaptive response mechanisms and activating the exit from quiescent state, through a complex network of finely regulated miRNA targets related to quiescence, transcription, and one-carbon pool metabolism. Consistent with these findings, SCs/CSCs display innate resistance to anti-folate chemotherapies either in vitro or in vivo that can be reversed by miR-146 depletion, unmasking a “hidden vulnerability” exploitable for the development of anti-CSC therapies.

In vitro and in vivo studies of gold(I) azolate/phosphane complexes for the treatment of basal like breast cancer

2018 ◽  
Vol 155 ◽  
pp. 418-427 ◽  
Author(s):  
Valentina Gambini ◽  
Martina Tilio ◽  
Eunice Wairimu Maina ◽  
Cristina Andreani ◽  
Caterina Bartolacci ◽  
...  
Keyword(s):  
Breast Cancer ◽  
In Vivo Studies ◽  
Basal Like Breast Cancer

scholarly journals Tumor Suppressor PLK2 May Serve as a Biomarker in Triple-Negative Breast Cancer for Improved Response to PLK1 Therapeutics

2021 ◽  
Vol 1 (3) ◽  
pp. 178-193
Author(s):  
Yang Gao ◽  
Elena B. Kabotyanski ◽  
Jonathan H. Shepherd ◽  
Elizabeth Villegas ◽  
Deanna Acosta ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Null Mouse ◽  
Chromosome 5Q ◽  
Basal Like Breast Cancer ◽  
Cycle Regulation

Polo-like kinase (PLK) family members play important roles in cell-cycle regulation. The founding member PLK1 is oncogenic and preclinically validated as a cancer therapeutic target. Paradoxically, frequent loss of chromosome 5q11–35, which includes PLK2, is observed in basal-like breast cancer. In this study, we found that PLK2 was tumor suppressive in breast cancer, preferentially in basal-like and triple-negative breast cancer (TNBC) subtypes. Knockdown of PLK1 rescued phenotypes induced by PLK2 loss both in vitro and in vivo. We also demonstrated that PLK2 directly interacted with PLK1 at prometaphase through the kinase but not the polo-box domains of PLK2, suggesting PLK2 functioned at least partially through the interaction with PLK1. Furthermore, an improved treatment response was seen in both Plk2-deleted/low mouse preclinical and patient-derived xenograft (PDX) TNBC models using the PLK1 inhibitor volasertib alone or in combination with carboplatin. Reexpression of PLK2 in an inducible PLK2-null mouse model reduced the therapeutic efficacy of volasertib. In summary, this study delineates the effects of chromosome 5q loss in TNBC that includes PLK2, the relationship between PLK2 and PLK1, and how this may render PLK2-deleted/low tumors more sensitive to PLK1 inhibition in combination with chemotherapy. Significance: The tumor-suppressive role of PLK2, and its relationship with oncogene PLK1, provide a mechanistic rationalization to use PLK1 inhibitors in combination with chemotherapy to treat PLK2-low/deleted tumors. TNBC, and other cancers with low PLK2 expression, are such candidates to leverage precision medicine to identify patients who might benefit from treatment with these inhibitors.

scholarly journals MELK is an oncogenic kinase essential for mitotic progression in basal-like breast cancer cells

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Yubao Wang ◽  
Young-Mi Lee ◽  
Lukas Baitsch ◽  
Alan Huang ◽  
Yi Xiang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Progesterone Receptors ◽  
Luminal Breast Cancer ◽  
Mouse Development ◽  
Basal Like Breast Cancer ◽  
Aggressive Subtype

Despite marked advances in breast cancer therapy, basal-like breast cancer (BBC), an aggressive subtype of breast cancer usually lacking estrogen and progesterone receptors, remains difficult to treat. In this study, we report the identification of MELK as a novel oncogenic kinase from an in vivo tumorigenesis screen using a kinome-wide open reading frames (ORFs) library. Analysis of clinical data reveals a high level of MELK overexpression in BBC, a feature that is largely dependent on FoxM1, a master mitotic transcription factor that is also found to be highly overexpressed in BBC. Ablation of MELK selectively impairs proliferation of basal-like, but not luminal breast cancer cells both in vitro and in vivo. Mechanistically, depletion of MELK in BBC cells induces caspase-dependent cell death, preceded by defective mitosis. Finally, we find that Melk is not required for mouse development and physiology. Together, these data indicate that MELK is a normally non-essential kinase, but is critical for BBC and thus represents a promising selective therapeutic target for the most aggressive subtype of breast cancer.

scholarly journals FGFR Signaling Promotes the Growth of Triple-Negative and Basal-Like Breast Cancer Cell Lines Both In Vitro and In Vivo

2011 ◽  
Vol 17 (16) ◽  
pp. 5275-5286 ◽  
Author(s):  
Rachel Sharpe ◽  
Alex Pearson ◽  
Maria T. Herrera-Abreu ◽  
Damian Johnson ◽  
Alan Mackay ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Triple Negative ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Basal Like Breast Cancer

Melatonin modifies tumor hypoxia and metabolism by inhibiting HIF-1α and energy metabolic pathway in the in vitro and in vivo models of breast cancer

2019 ◽  
Vol 2 (4) ◽  
pp. 83-98 ◽  
Author(s):  
André De Lima Mota ◽  
Bruna Vitorasso Jardim-Perassi ◽  
Tialfi Bergamin De Castro ◽  
Jucimara Colombo ◽  
Nathália Martins Sonehara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucose Metabolism ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Carbonic Anhydrases ◽  
In Vivo Models ◽  
Ca Ix ◽  
Gene And Protein Expression

Breast cancer is the most common cancer among women and has a high mortality rate. Adverse conditions in the tumor microenvironment, such as hypoxia and acidosis, may exert selective pressure on the tumor, selecting subpopulations of tumor cells with advantages for survival in this environment. In this context, therapeutic agents that can modify these conditions, and consequently the intratumoral heterogeneity need to be explored. Melatonin, in addition to its physiological effects, exhibits important anti-tumor actions which may associate with modification of hypoxia and Warburg effect. In this study, we have evaluated the action of melatonin on tumor growth and tumor metabolism by different markers of hypoxia and glucose metabolism (HIF-1α, glucose transporters GLUT1 and GLUT3 and carbonic anhydrases CA-IX and CA-XII) in triple negative breast cancer model. In an in vitro study, gene and protein expressions of these markers were evaluated by quantitative real-time PCR and immunocytochemistry, respectively. The effects of melatonin were also tested in a MDA-MB-231 xenograft animal model. Results showed that melatonin treatment reduced the viability of MDA-MB-231 cells and tumor growth in Balb/c nude mice (p <0.05). The treatment significantly decreased HIF-1α gene and protein expression concomitantly with the expression of GLUT1, GLUT3, CA-IX and CA-XII (p <0.05). These results strongly suggest that melatonin down-regulates HIF-1α expression and regulates glucose metabolism in breast tumor cells, therefore, controlling hypoxia and tumor progression. 

The truncated somatostatin receptor sst5TMD4 stimulates the production of pro-angiogenic factors in in vitro and in vivo breast cancer models

2014 ◽  
Author(s):  
Raul M Luque ◽  
Mario Duran-Prado ◽  
David Rincon-Fernandez ◽  
Marta Hergueta-Redondo ◽  
Michael D Culler ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Somatostatin Receptor ◽  
Angiogenic Factors ◽  
Cancer Models
Sign in / Sign up

Export Citation Format

Share Document