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Article Open Access

Differential response of MDA‑MB‑231 breast cancer and MCF10A normal breast cells to cytoskeletal disruption

  • Authors:
    • Sangwoo Kwon
    • Se Jik Han
    • Kyung Sook Kim
  • View Affiliations / Copyright

    Affiliations: Department of Biomedical Engineering, College of Medicine, Kyung Hee University, Seoul 02447, Republic of Korea
    Copyright: © Kwon et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 200
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    Published online on: September 29, 2023
       https://doi.org/10.3892/or.2023.8637
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Abstract

Metastasis remains a major clinical problem in cancer diagnosis and treatment. Metastasis is the leading cause of cancer‑related mortality but is still poorly understood. Cytoskeletal proteins are considered potential therapeutic targets for metastatic cancer cells because the cytoskeleton serves a key role in the migration and invasion of these cells. Vimentin and F‑actin exhibit several functional similarities and undergo quantitative and structural changes during carcinogenesis. The present study investigated the effects of vimentin and F‑actin deficiency on the survival and motility of breast cancer cells. In metastatic breast cancer cells (MDA‑MB‑231) and breast epithelial cells (MCF10A), vimentin was knocked down by small interfering RNA and F‑actin was depolymerized by latrunculin A, respectively. The effect of reduced vimentin and F‑actin content on cell viability was analyzed using the MTT assay and the proliferative capacity was compared by analyzing the recovery rate. The effect on motility was analyzed based on two processes: The distance traveled by tracking the cell nucleus and the movement of the protrusions. The effects on cell elasticity were measured using atomic force microscopy. Separately reducing vimentin or F‑actin did not effectively inhibit the growth and motility of MDA‑MB‑231 cells; however, when both vimentin and F‑actin were simultaneously deficient, MDA‑MB‑231 cells growth and migration were severely impaired. Vimentin deficiency in MDA‑MB‑231 cells was compensated by an increase in F‑actin polymerization, but no complementary action of vimentin on the decrease in F‑actin was observed. In MCF10A cells, no complementary interaction was observed for both vimentin and F‑actin.
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Copy and paste a formatted citation
Spandidos Publications style
Kwon S, Han SJ and Kim KS: Differential response of MDA‑MB‑231 breast cancer and MCF10A normal breast cells to cytoskeletal disruption. Oncol Rep 50: 200, 2023.
APA
Kwon, S., Han, S.J., & Kim, K.S. (2023). Differential response of MDA‑MB‑231 breast cancer and MCF10A normal breast cells to cytoskeletal disruption. Oncology Reports, 50, 200. https://doi.org/10.3892/or.2023.8637
MLA
Kwon, S., Han, S. J., Kim, K. S."Differential response of MDA‑MB‑231 breast cancer and MCF10A normal breast cells to cytoskeletal disruption". Oncology Reports 50.5 (2023): 200.
Chicago
Kwon, S., Han, S. J., Kim, K. S."Differential response of MDA‑MB‑231 breast cancer and MCF10A normal breast cells to cytoskeletal disruption". Oncology Reports 50, no. 5 (2023): 200. https://doi.org/10.3892/or.2023.8637
Copy and paste a formatted citation
x
Spandidos Publications style
Kwon S, Han SJ and Kim KS: Differential response of MDA‑MB‑231 breast cancer and MCF10A normal breast cells to cytoskeletal disruption. Oncol Rep 50: 200, 2023.
APA
Kwon, S., Han, S.J., & Kim, K.S. (2023). Differential response of MDA‑MB‑231 breast cancer and MCF10A normal breast cells to cytoskeletal disruption. Oncology Reports, 50, 200. https://doi.org/10.3892/or.2023.8637
MLA
Kwon, S., Han, S. J., Kim, K. S."Differential response of MDA‑MB‑231 breast cancer and MCF10A normal breast cells to cytoskeletal disruption". Oncology Reports 50.5 (2023): 200.
Chicago
Kwon, S., Han, S. J., Kim, K. S."Differential response of MDA‑MB‑231 breast cancer and MCF10A normal breast cells to cytoskeletal disruption". Oncology Reports 50, no. 5 (2023): 200. https://doi.org/10.3892/or.2023.8637
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