Hyaluronic Acid Improves Hydrogen Peroxide Modulatory Effects on Calcium Channel and Sodium-Potassium Pump in 4T1 Breast Cancer Cell Line

Maintaining homeostasis of ion concentrations is critical in cancer cells. Under hypoxia, the levels of channels and pumps in cancer cells are more active than normal cells suggesting ion channels as a suitable therapeutic target. One of the contemporary ways for cancer therapy is oxidative stress. However, the effective concentration of oxidative stress on tumor cells has been reported to be toxic for normal cells as well. In this study, we benefited from the modifying effects of hyaluronic acid (HA) on H2O2, as a free radical source, to make a gradual release of oxidative stress on cancer cells while preventing/decreasing damage to normal cells under normoxia and hypoxic conditions. To do so, we initially investigated the optimal concentration of HA antioxidant capacity by the DPPH test. In the next step, we found optimum H2O2 dose by treating the 4T1 breast cancer cell line with increasing concentrations (0, 10, 20, 50,100, 200, 500, and 1000 μM) of H2O2 alone or H2O2 + HA (83%) for 24 hrs. The calcium channel and the sodium-potassium pumps were then evaluated by measuring the levels of calcium, sodium, and potassium ions using an atomic absorption flame spectrophotometer. The results revealed that treatment with H2O2 or H2O2+ HA led to an intracellular increase of calcium, sodium, and potassium in the normoxic and hypoxic circumstances in a dose-dependent manner. It is noteworthy that H2O2 + HA treatment had more favorable and controllable effects compared with H2O2 alone. Moreover, HA optimizes the antitumor effect of oxidative stress exerted by H2O2 making H2O2 + HA suitable for clinical use in cancer treatment along with chemotherapy.

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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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Continuous Hypoxia and Glucose Metabolism, The Effects on Genes Expression in Mcf7 Breast Cancer Cell Line

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530320666200506082020 ◽

2020 ◽

Vol 20 ◽

Author(s):

Abdel Qader Al Bawab ◽

Malek Zihlif ◽

Yazan Jarrar ◽

Ahmad Saleh

Keyword(s):

Breast Cancer ◽

Glucose Metabolism ◽

Cancer Cells ◽

Cell Line ◽

Breast Cancer Cell Line ◽

Warburg Effect ◽

Cancer Cell Line ◽

Mcf7 Cells ◽

Genetic Changes ◽

Genes Expression

Background: Hypoxia (deprived oxygen in tissues) may induce molecular and genetic changes in cancer cells. Objective: Investigating the genetic changes of glucose metabolism in breast cancer cell line (MCF7) after exposure to continuous hypoxia (10 and 20 cycles exposure of 72 hours continuously on a weekly basis). Method: Gene expression of MCF7 cells was evaluated using real-time polymerase chain reaction- array method. Furthermore, cell migration and wound healing assays were also applied. Results: It was found that 10 episodes of continuous hypoxia activated Warburg effect in MCF7 cells via the significant up-regulation of genes involved in glycolysis (ANOVA, p value < 0.05). The molecular changes were associated with the ability of MCF7 cells to divide and migrate. Interestingly, after 20 episodes of continuous hypoxia, the expression glycolysis mediated genes has dropped significantly (from 30 to 9 folds). This could be attributed to the adaptive ability of cancer cells. Conclusion: It is concluded that 10 hypoxic episodes increased the survival rate and the aggressiveness of MCF7 cells and induced Warburg effect by up-regulation of the glycolysis mediating genes expression.

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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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Dexamethasone Reduces Cell Adhesion and Migration of T47D Breast Cancer Cell Line

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520621666201214150427 ◽

2020 ◽

Vol 21 ◽

Author(s):

Leila Mohammadi ◽

Bashir Mosayyebi ◽

Mahsa Imani ◽

Mohammad Rahmati

Keyword(s):

Breast Cancer ◽

Cell Adhesion ◽

Cancer Cells ◽

Cell Line ◽

Breast Cancer Cell Line ◽

Cell Adhesion Molecules ◽

Cancer Cell Line ◽

T47d Breast Cancer Cell ◽

Cell Adhesion And Migration ◽

And Migration

Background: Aberrant expression of cell adhesion molecules and matrix metalloproteinase (MMPs) plays a pivotal role in tumor biological processes including progression and metastasis of cancer cells. Targeting these processes and detailed understanding of their underlying molecular mechanism is an essential step in cancer treatment. Dexamethasone (Dex) is a type of synthetic corticosteroid hormone used as adjuvant therapy in combination with current cancer treatments such as chemotherapy in order to alleviate its side effects like acute nausea and vomiting. Recent evidences have suggested that Dex may have antitumor characteristics. Objective: Dex affects the migration and adhesion of T47D breast cancer cells as well as cell adhesion molecules e.g., cadherin and integrin, and MMPs by regulating the expression levels of associated genes. Methods: In this study, we evaluated the cytotoxicity of Dex on the T47D breast cancer cell line through MTT assay. Cell adhesion assay and wound healing assay were performed to determine the impact of Dex on cell adhesion and cell migration, respectively. Moreover, real-time PCR was used to measure the levels of α and β integrin, E-cadherin, N-cadherin, MMP-2, and MMP-9. Results: Dex decreased the viability of T47D cells in a time and dose-dependent manner. Cell adhesion and migration of T47D cells were reduced upon Dex treatment. The expression of α and β integrin, E-cadherin, N-cadherin, MMP-2, and MMP-9 were altered in response to the Dex treatment. Conclusion: Our findings demonstrated that Dex may have a role in the prevention of metastasis in this cell line.

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c-myb mediates inflammatory reaction against oxidative stress in human breast cancer cell line, MCF-7

Cell Biochemistry and Function ◽

10.1002/cbf.1808 ◽

2011 ◽

Vol 29 (8) ◽

pp. 686-693 ◽

Cited By ~ 8

Author(s):

Govinda Bhattarai ◽

Young-Hee Lee ◽

Nan-Hee Lee ◽

Ji-Soo Yun ◽

Pyoung-Han Hwang ◽

...

Keyword(s):

Breast Cancer ◽

Oxidative Stress ◽

Cell Line ◽

Inflammatory Reaction ◽

Breast Cancer Cell Line ◽

Human Breast Cancer ◽

Cancer Cell Line ◽

Human Breast Cancer Cell ◽

Human Breast ◽

Mcf 7

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Hyaluronic acid as drug delivery for sodium butyrate: Improvement of the anti-proliferative activity on a breast-cancer cell line

International Journal of Cancer ◽

10.1002/(sici)1097-0215(19990505)81:3<411::aid-ijc15>3.0.co;2-f ◽

1999 ◽

Vol 81 (3) ◽

pp. 411-416 ◽

Cited By ~ 76

Author(s):

Danila Coradini ◽

Cinzia Pellizzaro ◽

Giuliana Miglierini ◽

Maria Grazia Daidone ◽

Alberto Perbellini

Keyword(s):

Breast Cancer ◽

Drug Delivery ◽

Hyaluronic Acid ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Sodium Butyrate ◽

Breast Cancer Cell Line ◽

Proliferative Activity ◽

Cancer Cell Line

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Anticancer tendency of aflatoxin B1 in 4T1 breast cancer cell line

Gene Reports ◽

10.1016/j.genrep.2019.100442 ◽

2019 ◽

Vol 16 ◽

pp. 100442 ◽

Cited By ~ 1

Author(s):

Roya Mousazadeh ◽

Saeed Hesaraki ◽

Mansour Bayat ◽

Alireza Jahandideh ◽

Jamal Hashemi

Keyword(s):

Breast Cancer ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Aflatoxin B1 ◽

Cancer Cell Line ◽

4T1 Breast Cancer

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Long Noncoding RNA CAMTA1 Promotes Proliferation and Mobility of the Human Breast Cancer Cell Line MDA-MB-231 via Targeting miR-20b

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics ◽

10.3727/096504017x14953948675395 ◽

2018 ◽

Vol 26 (4) ◽

pp. 625-635 ◽

Cited By ~ 3

Author(s):

Pengwei Lu ◽

Yuanting Gu ◽

Lin Li ◽

Fang Wang ◽

Xue Yang ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cell Line ◽

Long Noncoding Rna ◽

Human Breast Cancer ◽

Noncoding Rna ◽

Breast Cancer Cells ◽

Cancer Cell Line ◽

Human Breast Cancer Cell ◽

Human Breast

Breast cancer is a serious threat to women’s physical and psychological health. Long noncoding RNA CAMTA1 (lncCAMTA1) was believed to be related with tumor progression, but its role in breast cancer is not clear. The human breast cancer cell line MDA-MB-231 was used to investigate the effect of lncCAMTA1 on cell viability, migration/invasion, and apoptosis. The expression of lncCAMTA1, miR-20b, and VEGF in MDA-MB-231 were measured after corresponding transfections. Binding effects between lncCAMTA1 and miR-20b, miR-20b, and VEGF 3′-UTR were measured. The effects of miR-20b and VEGF on breast cancer cells were also assessed after transfections. The phosphorylation levels of the MAPK/ERK and JAK/STAT3 pathways were determined to assess the effect of VEGF. The results showed that lncCAMTA1 expression promoted cell viability and migration/invasion, while knockdown of lncCAMTA1 promoted cell apoptosis via binding with miR-20b. lncCAMTA1 negatively regulated miR-20b expression. VEGF was a target of miR-20b, leading to the modification of the phosphorylation levels of MAPK, ERK, JAK, STAT1, and STAT3. Our findings suggested that lncCAMTA1 might promote proliferation and mobility of human breast cancer cells via binding with miR-20b. VEGF was a direct target of miR-20b and regulated activation of the MAPK/ERK and JAK/STAT3 signaling pathways. Therefore lncCAMTA1 has potential as a novel cancer diagnostic marker and as a putative novel therapeutic target for breast cancer treatment.

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