scholarly journals Interaction of platelet-derived autotaxin with tumor integrin αVβ3 controls metastasis of breast cancer cells to bone

Blood ◽  
2014 ◽  
Vol 124 (20) ◽  
pp. 3141-3150 ◽  
Author(s):  
Raphael Leblanc ◽  
Sue-Chin Lee ◽  
Marion David ◽  
Jean-Claude Bordet ◽  
Derek D. Norman ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Integrin Αvβ3 ◽  
Skeletal Metastases ◽  
Key Points ◽  
Induced Aggregation

Key Points ATX stored in α-granules of resting platelets is secreted upon tumor cell-induced aggregation leading to prometastatic LPA production. Nontumoral ATX promotes early bone colonization by breast cancer cells and contributes to the progression of skeletal metastases.

scholarly journals A Nuclear-Directed Ribonuclease Variant Targets Cancer Stem Cells and Inhibits Migration and Invasion of Breast Cancer Cells

Cancers ◽  
2021 ◽  
Vol 13 (17) ◽  
pp. 4350
Author(s):  
Jessica Castro ◽  
Giusy Tornillo ◽  
Gerardo Ceada ◽  
Beatriz Ramos-Neble ◽  
Marlon Bravo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Migration And Invasion ◽  
Tumor Cell Lines

Despite the significant advances in cancer research made in recent years, this disease remains one of the leading causes of death worldwide. In part, this is due to the fact that after therapy, a subpopulation of self-renewing tumor cells can survive and promote cancer relapse, resistance to therapies and metastasis. Targeting these cancer stem cells (CSCs) is therefore essential to improve the clinical outcome of cancer patients. In this sense, multi-targeted drugs may be promising agents targeting CSC-associated multifocal effects. We have previously constructed different human pancreatic ribonuclease (RNase) variants that are cytotoxic for tumor cells due to a non-classical nuclear localization signal introduced in their sequence. These cytotoxic RNases affect the expression of multiple genes involved in deregulated metabolic and signaling pathways in cancer cells and are highly cytotoxic for multidrug-resistant tumor cell lines. Here, we show that these cytotoxic nuclear-directed RNases are highly selective for tumor cell lines grown in 3D, inhibit CSCs’ development and diminish the self-renewal capacity of the CSCs population. Moreover, these human RNase variants reduce the migration and invasiveness of highly invasive breast cancer cells and downregulate N-cadherin expression.

Effect of IL-8 on integrin αvβ3 expression and cell motility via PI3K, Akt, and NF-κB-dependent pathway in human breast cells.

2012 ◽  
Vol 30 (27_suppl) ◽  
pp. 158-158
Author(s):  
Nan Shao ◽  
Shenming Wang ◽  
Yunjian Zhang ◽  
Ying Lin
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Signal Transduction Pathway ◽  
Integrin Αvβ3 ◽  
Αvβ3 Integrin ◽  
Blocking Antibody ◽  
Cancer Aggressiveness ◽  
The Status ◽  
Breast Cells

158 Background: αvβ3 integrin-overexpression in tumor associated vasculature is a marker of poor prognosis in breast cancer. A positive correlation between αvβ3 integrin and overexpression of Interleukin-8 (IL-8), a multifunctional cytokine associated with breast cancer aggressiveness was recently demonstrated. Here, we addressed the effects of IL-8 in migration and integrin expression in breast cancer cells. Methods: The IL-8 overexpressing breast cancer cells MDA-MB-231 and HS 578t were treated with IL-8 siRNA and evaluated for cells motility and alterations in the expression of αvβ3. Western Blotting to identify the status of PI3K, Akt and NF-κB. Results: In this study, we found that αvβ3 expression was decreased by IL-8 siRNA, especially the expression of β3. Treatment with αvβ3-blocking antibody LM609 and β3 siRNA significantly reduced invasion in the IL-8 overexpressing cells MDA-MB-231 and HS 578t. The phosphorylation of PI3K, Akt and NF-κB was abrogated after IL-8 siRNA treatment. The IL-8 siRNA can also decrease the binding of β3 promoter and the NF-κB-P65. Conclusions: These results indicate that IL-8 enhances the motility of highly invasive breast cancer cells by regulating αvβ3 expression partially through PI3K/Akt/ NF-κB signal transduction pathway.

scholarly journals Enhancement of Tumor Cell Death by Combining gef Gene Mediated Therapy and New 1,4-Benzoxazepin-2,6-Dichloropurine Derivatives in Breast Cancer Cells

2018 ◽  
Vol 9 ◽  
Author(s):  
Alberto Ramírez ◽  
Ana Conejo-García ◽  
Carmen Griñán-Lisón ◽  
Luisa C. López-Cara ◽  
Gema Jiménez ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tumor Cell Death

scholarly journals Integrin αvβ3 in the Mediating Effects of Dihydrotestosterone and Resveratrol on Breast Cancer Cell Proliferation

2020 ◽  
Vol 21 (8) ◽  
pp. 2906
Author(s):  
Yih Ho ◽  
Zi-Lin Li ◽  
Ya-Jung Shih ◽  
Yi-Ru Chen ◽  
Kuan Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Plasma Membrane ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Integrin Αvβ3 ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation

Hormones and their receptors play an important role in the development and progression of breast cancer. Hormones regulate the proliferation of breast cancer cells through binding between estrogen or progestins and steroid receptors that may reside in the cytoplasm or be transcriptionally activated as steroid–protein nuclear receptor complexes. However, receptors for nonpeptide hormones also exist in the plasma membrane. Via those receptors, hormones are able to stimulate breast cancer cell proliferation when activated. Integrins are heterodimeric structural proteins of the plasma membrane. Their primary functions are to interact with extracellular matrix proteins and growth factors. Recently, integrin αvβ3 has been identified as a receptor for nonpeptide hormones, such as thyroid hormone and dihydrotestosterone (DHT). DHT promotes the proliferation of human breast cancer cells through binding to integrin αvβ3. A receptor for resveratrol, a polyphenol stilbene, also exists on this integrin in breast cancer cells, mediating the anti-proliferative, pro-apoptotic action of the compound in these cells. Unrelated activities of DHT and resveratrol that originate at integrin depend upon downstream stimulation of mitogen-activated protein kinase (MAPK, ERK1/2) activity, suggesting the existence of distinct, function-specific pools of ERK1/2 within the cell. This review will discuss the features of these receptors in breast cancer cells, in turn suggesting clinical applications that are based on the interactions of resveratrol/DHT with integrin αvβ3 and other androgen receptors.

Immunomagnetic Tumor Cell Enrichment Is Promising in Detecting Circulating Breast Cancer Cells

Oncology ◽  
2003 ◽  
Vol 64 (2) ◽  
pp. 160-165 ◽  
Author(s):  
X.C. Hu ◽  
Y. Wang ◽  
D.R. Shi ◽  
T.Y. Loo ◽  
L.W.C. Chow
Keyword(s):  
Breast Cancer ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cell Enrichment

Antitumor effects of zoledronic acid in combination with histone deacetylase inhibitor valproic acid.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e15158-e15158
Author(s):  
Arne Strauß ◽  
Hagen Loertzer ◽  
Rolf-Hermann Ringert ◽  
Paul Thelen
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Valproic Acid ◽  
Zoledronic Acid ◽  
Tumor Cell ◽  
Cell Viability ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Antitumor Effects ◽  
Mcf 7

e15158 Background: The established utilisation of bisphosphonates is the treatment of metastatic bone disease derived from several tumor types including prostate (PCa) and breast cancer. However, recently preclinical as well as clinical evidence support anti-tumor activities of these drugs in their own right. To probe into the molecular basis of such observations we treated PCa bone metastasis derived cell lines (VCaP, PC-3) and breast cancer cells (MCF-7) with zoledronic acid (ZA) and ZA in combination with valproic acid (VPA). HDAC-Inhibitor VPA according to our previous findings rectifies aberrant androgen receptor signalling and thus, implies an anti-androgen element in these treatments. Methods: PCa cells (VCaP, PC-3) and breast cancer cells (MCF-7) were treated with ZA (Zometa, Novartis) at 0, 5, 25 or 100µM or same ZA concentrations in combination with VPA (5mM). Tumor cell viability and proliferation were analysed by AlamarBlue- and BrdU-tests. Gene expression and PSA secretion was quantitated by real time RT-PCR and was further assessed with ELISA-kits, respectively. Results: In all cell types ZA has no impact on tumor cell viability or proliferation of its own exceeding the effects of VPA alone. Likewise, PSA secretion in VCaP cells is not further diminished in the combined ZA/VPA treatments. However, among a marked impact on cancer relevant gene expression protective elements such as vitamin D- and β-estrogen-receptor are up-regulated by ZA alone and in excess by the combined treatment. Other genes associated with protective features such as IGFBP-3, SOCS-3 and Se-BP-3 are up-regulated only by the ZA/VPA combination. Conclusions: We present molecular evidence for anti-tumor effects of zoledronic acid. Our data suggest the necessity of a concomitant anti-androgen treatment for maximal benefit. The genes addressed by such treatments are more associated with cancer prevention than immediate androgen signalling targets. Therefore, the main anti-tumor potential of ZA may emerge from an early onset of combined therapies to prevent bone metastases.

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