Quercetin Enhances the Suppressive Effects of Doxorubicin on the Migration of MDA-MB-231 Breast Cancer Cell Line

Background: Cancer cell metastasis is facilitated by matrix-metalloproteinases through degradation of extracellular matrix (ECM) proteins and is a major cause of mortality. One of the most common remedies for cancer is chemotherapy, which has many side effects. Therefore, it seems necessary to find a way to reduce the side effects of these drugs while maintaining their anticancer effects. Quercetin (que) is a natural substance that has been reported to have anticancer activities. Objectives: This study aims at evaluating the effect of que in combination with doxorubicin (dox) on the migration of the MDA-MB-231 breast cancer cell line. Methods: The effects of que and dox on cell viability in 24h and 48 h was assessed by MTT assay. Also, the effects of the same drugs on the cancer cells migration were evaluated, using the wound healing assay. Lastly, the effects of que and dox were assessed on the expression of MMP-2 and MMP-9 genes. Results: The combination of 50 µM of que with 32 nM of dox was selected by CI comparison. The viability and migration of cancer cells and the gelatinases genes expression were decreased after treatment with individual drugs. The migration and the expression of MMP-2 and MMP-9 genes after treatment with the combination of que and dox was significantly reduced compared to the treatment with que and dox alone. Conclusions: Que inhibits the viability and migration of MDA-MB-231 cancer cells and synergistically enhances the effects of dox on the survival and migration of these cells. Hence, we propose this drug combination as a path for further research on breast cancer therapy.

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Seeding of breast cancer cell line (MDA-MB-231LUC+) to the mandible induces overexpression of substance P and CGRP throughout the trigeminal ganglion and widespread peripheral sensory neuropathy throughout all three of its divisions

Molecular Pain ◽

10.1177/17448069211024082 ◽

2021 ◽

Vol 17 ◽

pp. 174480692110240

Author(s):

Silvia Gutierrez ◽

James C Eisenach ◽

M Danilo Boada

Keyword(s):

Breast Cancer ◽

Substance P ◽

Cancer Cells ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Trigeminal Ganglion ◽

Breast Cancer Cell Line ◽

Cancer Cell Line ◽

The Impact

Some types of cancer are commonly associated with intense pain even at the early stages of the disease. The mandible is particularly vulnerable to metastasis from breast cancer, and this process has been studied using a bioluminescent human breast cancer cell line (MDA-MB-231LUC+). Using this cell line and anatomic and neurophysiologic methods in the trigeminal ganglion (TG), we examined the impact of cancer seeding in the mandible on behavioral evidence of hypersensitivity and on trigeminal sensory neurons. Growth of cancer cells seeded to the mandible after arterial injection of the breast cancer cell line in Foxn1 animals (allogeneic model) induced behavioral hypersensitivity to mechanical stimulation of the whisker pad and desensitization of tactile and sensitization of nociceptive mechanically sensitive afferents. These changes were not restricted to the site of metastasis but extended to sensory afferents in all three divisions of the TG, accompanied by widespread overexpression of substance P and CGRP in neurons through the ganglion. Subcutaneous injection of supernatant from the MDA-MB-231LUC+ cell culture in normal animals mimicked some of the changes in mechanically responsive afferents observed with mandibular metastasis. We conclude that released products from these cancer cells in the mandible are critical for the development of cancer-induced pain and that the overall response of the system greatly surpasses these local effects, consistent with the widespread distribution of pain in patients. The mechanisms of neuronal plasticity likely occur in the TG itself and are not restricted to afferents exposed to the metastatic cancer microenvironment.

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Neuropeptide Y stimulates proliferation and migration in the 4T1 breast cancer cell line

International Journal of Cancer ◽

10.1002/ijc.26350 ◽

2011 ◽

Vol 131 (2) ◽

pp. 276-286 ◽

Cited By ~ 23

Author(s):

Philip J. Medeiros ◽

Baraa K. Al-Khazraji ◽

Nicole M. Novielli ◽

Lynne M. Postovit ◽

Ann F. Chambers ◽

...

Keyword(s):

Breast Cancer ◽

Neuropeptide Y ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Cancer Cell Line ◽

4T1 Breast Cancer ◽

And Migration ◽

Proliferation And Migration

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The Effect of Duloxetine on Tau Protein and Migration in Breast Cancer Cell Line

International Journal of Cancer Management ◽

10.5812/ijcm.6422 ◽

2017 ◽

Vol 10 (5) ◽

Author(s):

Bahareh Zarrin ◽

Shaghayegh Haghjooy Javanmard ◽

Fariba Samani ◽

Mohamadhasan Tajadini ◽

Maryam Jamady ◽

...

Keyword(s):

Breast Cancer ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Tau Protein ◽

Cancer Cell Line ◽

And Migration

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Silibinin Inhibit Cell Migration through Downregulation of RAC1 Gene Expression in Highly Metastatic Breast Cancer Cell Line

Drug Research ◽

10.1055/a-1223-1734 ◽

2020 ◽

Vol 70 (10) ◽

pp. 478-483

Author(s):

Hamed Esmaeil Lashgarian ◽

Vahid Adamii ◽

Vajihe Ghorbanzadeh ◽

Leila Chodari ◽

Fayze Kamali ◽

...

Keyword(s):

Breast Cancer ◽

Cell Line ◽

Tumor Cells ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Cancer Cell Line ◽

Migration And Invasion ◽

And Migration ◽

Proliferation And Migration

Abstract Background Triple negative breast cancer is the most invasive breast cancer subtype and possesses poor prognosis and survival. Rho GTPase famil, especially Rac1 participates in a number of signaling events in cells with crucial roles in malignancy, migration and invasion of tumor cells. Silibinin, a flavonoid antioxidant from milk thistle has attracted attention in the recent decades for chemoprevention and chemotherapy of tumor cells. In this study, the effect of silibinin on the migration capacity of MDA-MB-231 cells, a highly metastatic human breast cancer cell line was investigated by evaluation of Rac1 expression. Method MTT wound healing and transwell assays were performed to evaluate the effects of silibinin on proliferation and migration of MDA-MB-231 cells. In addition, the influence of the silibinin on the expression of Rac1mRNAs was assessed by RT-PCR. Results Results indicated significant dose-dependent inhibitory effect of silibinin on proliferation and migration of MDA-MB-231 cells. It significantly inhibited the expression of Rac1 mRNA. Conclusion In conclusion, the results demonstrate that the silibinin can be used as an experimental therapeutic for the management of TNBC metastatic cancer.

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Effect of CD44 Aptamer on Snail Metastasis Factor and Aggressiveness of MDA-MB-231 Breast Cancer Cell Line

Shiraz E-Medical Journal ◽

10.5812/semj.94641 ◽

2020 ◽

Vol 21 (5) ◽

Author(s):

Soudabeh Kavousipour ◽

Pooneh Mokarram ◽

Mahdi Barazesh ◽

Elham Arabizadeh ◽

Vahid Razban ◽

...

Keyword(s):

Breast Cancer ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Cancer Cell Line ◽

Invasive Behavior ◽

And Migration ◽

2D And 3D ◽

Aggressive Breast Cancer

Background: The intracellular signaling pathways stimulated by CD44/hyaluronic acid (HA) interaction play a central role in the invasion and migration of cancer cells. Epithelial-mesenchyme transition (EMT) is an important factor in cancer metastasis and migration, which can be stimulated by the snail transcription factor. Previous studies showed cells that were subjected to snail-induced EMT, characterized by a CD44high/CD24low phenotype, expressed at their surface. Objectives: The aim of this study was to assess the inhibitory effect of CD44/HA interaction on the snail expression and invasive behavior of aggressive breast cancer cell line with a high CD44 expression in 2D and 3D culture. The cell surface binding capacity of the selected aptamer was evaluated via flow cytometry assay. Methods: To test our hypothesis, we disrupted the CD44/HA interaction by DNA aptamer, which specifically binds to the Hyaluronic Acid Binding Domain (HABD) of CD44. Then, expression level of snail mRNA was evaluated in MDA-MB 231 cells, cultured in 2D and 3D conditions by real-time PCR. Furthermore, invasive behavior was evaluated, using wound healing assay. Results: The results of this study showed that CD44 aptamer reduced snail expression and invasive behavior in MDA-MB 231 cell line. In addition, our result indicated that cells cultured in 3D were more sensitive to the aptamer in comparison to those cultured in the 2D model. Conclusions: The inhibition of CD44-HA interaction, using aptamer, negatively regulates the CD44 function in aggressive breast cancer cell line with the high level of CD44 expression.

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The Cytotoxicity of Doxorubicin Can Be Accelerated by a Combination of Hyperthermia and 5-Aminolevulinic Acid

Antioxidants ◽

10.3390/antiox10101531 ◽

2021 ◽

Vol 10 (10) ◽

pp. 1531

Author(s):

Hiromi Kurokawa ◽

Hirofumi Matsui

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Aminolevulinic Acid ◽

Cancer Cell Line ◽

Efflux Transporter ◽

Normal Cells

Chemotherapy is cytotoxic to various cancer cells and as well as normal cells. Thus, treatments that demonstrate selective cytotoxicity for cancer cells are desired. The combination of chemotherapy and other cancer therapies can show synergic cytotoxicity, which may be a clue to the nature of the involved cancer cellar-specific damage. We previously reported a phenomenon whereby mitochondrial reactive oxygen species (mitROS) regulate the expression transporters involved in anticancer drug transport and mitROS production is increased by hyperthermia. Moreover, the uptake of 5-aminolevulinic acid (ALA) was enhanced by the increase in mitROS production. In this study, we investigated whether the combination of hyperthermia and ALA can enhance the cytotoxicity of doxorubicin. MitROS production and ALA-derived porphyrin accumulation by hyperthermia (HT) were increased in a murine breast cancer cell line. The expression of solute carrier 15A1 (SLC15A1) upregulated and an ATP-binding cassette subfamily G member 2 (ABCG2) downregulated by HT. Since SLC15A1 is an accumulating transporter for ALA, while ABCG2 is a porphyrin efflux transporter, porphyrin accumulation was enhanced. ABCG2 is also a doxorubicin efflux transporter. Thus, ALA treatment accelerates the intracellular concentration of porphyrin, which acts as a competitive inhibitor of doxorubicin. Indeed, the amount of intracellular doxorubicin was increased by a combination of HT and ALA. The cytotoxicity of doxorubicin was also enhanced. This enhancement was observed in the human breast cancer cell line while it was not seen in normal cells. The combination of HT and ALA treatment can enhance the cancer-specific cytotoxicity of doxorubicin.

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Investigation of the anti-cancer effects of free and PLGA-PAA encapsulated Hydroxytyrosol on the MCF-7 breast cancer cell line

Current Molecular Medicine ◽

10.2174/1566524020666201231103826 ◽

2020 ◽

Vol 20 ◽

Author(s):

Maryam Safi ◽

Habib Onsori ◽

Mohammad Rahmati

Keyword(s):

Breast Cancer ◽

Cyclin D1 ◽

Cancer Cells ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Cancer Cell Line ◽

Anti Cancer ◽

Mcf 7

Purpose: Breast cancer is the most frequent cancer among women and the most important cause of death. Surgery and chemotherapy are the common treatment of the breast cancer, but increasing drug resistance has created many challenges in its treatment. The present study aimed to investigate the anti-cancer function of free and nano-encapsulated hydroxytyrosol on the MCF-7 breast cancer cell line. Methods: The poly lactide-co-glycolide-co-polyacrylic acid (PLGA-co-PAA) nano-encapsulated Hydroxytyrosol was synthesized, and the MTT assay was performed to evaluate the anti-proliferative and anti-tumor effects of both free and nanoencapsulated Hydroxytyrosol. After the extraction of RNA from the treated and control cancer cells, cDNA synthesis was performed and the expression of P21, P27, and Cyclin D1 genes were evaluated by Real-Time PCR. Results: The results of the study showed that free (12 ppm and 72 hours) and nano-encapsulate (10 ppm and 24 hours) hydroxytyrosol resulted in 50% death (IC50) of the cancer cells and increased by increasing the concentration and time. Also, free and nano-encapsulated hydroxytyrosol increased the expression of P21 and P27 genes and reduced the expression of Cyclin D1 in breast cancer cells. In general, the nano-encapsulated hydroxytyrosol showed more anticancer function than the free hydroxytyrosol. Conclusion: The present study illustrated that the hydroxytyrosol could lead to the cell death in MCF-7 breast cancer by regulating the cell cycle. Also, the nano-encapsulation of Hydroxytyrosol enhanced the Hydroxytyrosol anticancer function by PLGA-co-PAA. However, for more accurate results, further studies on animal models are necessary.

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Effects of Metformin on Human Bone-derived Mesenchymal Stromal Cell – Breast Cancer Cell Line Interactions

10.21203/rs.3.rs-1173554/v1 ◽

2021 ◽

Author(s):

Maryana Teufelsbauer ◽

Clemens Lang ◽

Adelina Plangger ◽

Barbara Rath ◽

Doris Moser ◽

...

Keyword(s):

Breast Cancer ◽

Cell Line ◽

Cell Lines ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Cancer Cell Line ◽

Cancer Cell Lines ◽

Breast Cancer Cell Lines ◽

And Migration

Abstract Metformin is used to treat patients with type 2 diabetes mellitus and was found to lower the incidence of cancer. Bone metastasis is a common complication of advanced breast cancer. The present study investigated the effects of metformin on human bone-derived mesenchymal stromal cells (BM-MSC) – breast cancer cell line interactions. BM-MSCs grown from box chisels were tested for growth-stimulating and migration-controlling activity on four breast cancer cell lines either untreated or after pretreatment with metformin. Growth stimulation was tested in MTT tests and migration in scratch assays. Furthermore, the expression of adipokines of BM-MSCs in response to metformin was assessed using Western blot arrays. Compared to breast cancer cell lines (3.6 ± 1.4% reduction of proliferation), 500 µM metformin significantly inhibited the proliferation of BM-MSC lines (12.3 ± 2.2 reduction). Pretreatment of BM-MSCs with metformin showed variable effects of the resulting conditioned media (CM) on breast cancer cell lines depending on the specific BM-MSC –cancer line combination. Metformin significantly impaired the migration of breast cancer cell lines MDA-MB-231 and MDA-MB-436 in response to CM of drug-pretreated BM-MSCs. Assessment of metformin-induced alterations in expression of adipokines by BM-MSC CM indicated increased osteogenic signaling and possibly impairment of metastasis. In conclusion, the anticancer activities of metformin are the result of a range of direct and indirect mechanisms that lower tumor proliferation and progression. A lower metformin-induced protumor activity of BM-MSCs in the bone microenvironment seem to contribute to the positive effects of the drug in selected breast cancer patients.

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