Metformin resistant MDA-MB-468 cells exhibit EMT-like phenotype and increased migration capacity

Koker, Sahika Cingir; Yalcin, Banu; Turaçlı, İrem Doğan

doi:10.1007/s11033-022-07381-6

Cited by 4 publications

(4 citation statements)

References 62 publications

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“…MDA-MB-231 cell line (HTB-26 TM , American Type Culture Collection ® , USA) [ 62 , 63 ] was used, which was originally derived from a 51-year-old white American woman with metastatic breast cancer [ 64 ]. MDA-MB-231 cells are spindle-like in shape with a mean diameter of 18–20 µm [ 65 ], as shown in Figure 2A and B .…”

Section: Methodsmentioning

confidence: 99%

“…Electroporation can minimize drug concentration and side effects on the surrounding tissues by improving drug efficacy [56]. Prior studies suggest that electroporation techniques can be effectively combined with various drugs to improve therapeutic efficacy [57][58][59][60][61]. This research examined the efficacy of a combination of Met with EP using various assays.…”

Section: Introductionmentioning

confidence: 99%

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Efficacy of metformin and electrical pulses in breast cancer MDA-MB-231 cells

Sahu,

Camarillo,

Sundararajan

2024

Exploration of Targeted Anti-Tumor Therapy

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Aim: Triple-negative breast cancer (TNBC) is a very aggressive subset of breast cancer, with limited treatment options, due to the lack of three commonly targeted receptors, which merits the need for novel treatments for TNBC. Towards this need, the use of metformin (Met), the most widely used type-2 diabetes drug worldwide, was explored as a repurposed anticancer agent. Cancer being a metabolic disease, the modulation of two crucial metabolites, glucose, and reactive oxygen species (ROS), is studied in MDA-MB-231 TNBC cells, using Met in the presence of electrical pulses (EP) to enhance the drug efficacy. Methods: MDA-MB-231, human TNBC cells were treated with Met in the presence of EP, with various concentrations Met of 1 mmol/L, 2.5 mmol/L, 5 mmol/L, and 10 mmol/L. EP of 500 V/cm, 800 V/cm, and 1,000 V/cm (with a pulse width of 100 µs at 1 s intervals) were applied to TNBC and the impact of these two treatments was studied. Various assays, including cell viability, microscopic inspection, glucose, ROS, and wound healing assay, were performed to characterize the response of the cells to the combination treatment. Results: Combining 1,000 V/cm with 5 mmol/L Met yielded cell viability as low as 42.6% at 24 h. The glucose level was reduced by 5.60-fold and the ROS levels were increased by 9.56-fold compared to the control, leading to apoptotic cell death. Conclusions: The results indicate the enhanced anticancer effect of Met in the presence of electric pulses. The cell growth is inhibited by suppressing glucose levels and elevated ROS. This shows a synergistic interplay between electroporation, Met, glucose, and ROS metabolic alterations. The results show promises for combinational therapy in TNBC patients.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Efficacy of metformin and electrical pulses in breast cancer MDA-MB-231 cells

Sahu,

Camarillo,

Sundararajan

2024

Exploration of Targeted Anti-Tumor Therapy

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“…Mesenchymal cells contribute to the development of drug resistance. EMT plays an integral role in the migration and invasion of the epithelial cells and shows an important contribution pathologically to cancer progression [ 96 ]. It mainly manifests through decreasing the epithelial marker E-cadherin and increasing mesenchymal markers Vimentin and N -cadherin.…”

Section: Molecular Mechanisms Of Drug Resistance In Cancermentioning

confidence: 99%

Research Progress of Plant-Derived Natural Products against Drug-Resistant Cancer

Liu,

Wang,

Xia

et al. 2024

Nutrients

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As one of the malignant diseases globally, cancer seriously endangers human physical and mental health because of its high morbidity and mortality. Conventional cancer treatment strategies, such as surgical resection and chemoradiotherapy, are effective at the early stage of cancer but have limited efficacy for advanced cancer. Along with cancer progress and treatment, resistance develops gradually within the population of tumor cells. As a consequence, drug resistance become the major cause that leads to disease progression and poor clinical prognosis in some patients. The mechanisms of cancer drug resistance are quite complex and involve various molecular and cellular mechanisms. Therefore, exploring the mechanisms and finding specific targets are becoming imperative to overcome drug resistance. In recent years, plant-derived natural products have been evaluated as potential therapeutic candidates against cancer with drug resistance due to low side effects and high anticancer efficacy. A growing number of studies have shown that natural products can achieve superior antitumor effects through multiple signaling pathways. The mechanisms include regulation of multiple drug resistance (MDR)-related genes, inhibition of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway, induction of autophagy, and blockade of the cell cycle. This paper reviews the molecular and cellular mechanisms of cancer drug resistance, as well as the therapeutic effects and mechanisms of plant-derived natural products against cancer drug resistance. It provides references for developing therapeutic medication for drug-resistant cancer treatment with high efficacy and low side effects.

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“…It exhibits phenotypes that resemble basal-like breast cancer, a sub-type typically associated with TNBC. The cells are highly proliferative and invasive [18] and have been instrumental in advancing our knowledge of TNBC as well as the development of novel treatment strategies for this challenging disease [19].…”

Section: Introductionmentioning

confidence: 99%

Fetuin-A Modulates Tumor Growth and Invasion in a Basal-Like Triple Negative Breast Cancer Cell Line, MDA-MB-468

Kenchappa,

Korolkova,

Odiase

et al. 2023

Preprint

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The present studies were undertaken to address the role of fetuin-A in the growth and invasion potential in a triple negative breast cancer (TNBC) cell line, MDA-MB-468. Basal like TNBC that express high levels of ectopic fetuin-A have poorer prognosis for the patients compared to those that express low levels of the protein. We overexpressed fetuin-A in MDA-MB-468 and then determined the invasive potential of fetuin-A overexpressing cells vs controls transfected with empty vector. We also determined the adhesion and growth potential of the cells in the presence of only fetuin-A in serum free medium and also in complete medium. Our data suggest that fetuin-A overexpression significantly enhances the invasive potential of the cells and also the expression of Toll like receptor 4 (TLR4) on these cells. More importantly, the cells rely on fetuin-A-TLR4 signaling network for growth and invasion because the specific TLR4 inhibitor CLI-095 (resatorvid) abrogates fetuin-A mediated growth and invasion. Taken together, the data suggest that fetuin-A-TLR4 signaling network plays a significant role in the growth and invasion potential of TNBC.

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Metformin resistant MDA-MB-468 cells exhibit EMT-like phenotype and increased migration capacity

Cited by 4 publications

References 62 publications

Efficacy of metformin and electrical pulses in breast cancer MDA-MB-231 cells

Efficacy of metformin and electrical pulses in breast cancer MDA-MB-231 cells

Research Progress of Plant-Derived Natural Products against Drug-Resistant Cancer

Fetuin-A Modulates Tumor Growth and Invasion in a Basal-Like Triple Negative Breast Cancer Cell Line, MDA-MB-468

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