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Amikacin Suppresses Human Breast Cancer Cell MDA-MB-231 Migration and Invasion
Yun-Hsin Wang1,2, Yau-Hung Chen2, Wen-Hao Shen1
1Division of Basic Research, Koo Foundation Sun Yat-Sen Cancer Center, Taipei 112, Taiwan.
Abstract:
(1) Background: Amikacin is an aminoglycoside antibiotic used for treating gram-negative bacterial infections in cancer patients. In this study, our aims are to investigate the migratory inhibition effects of amikacin in human MDA-MB-231 cells. (2) Methods: We used a wound-healing assay, trans-well analysis, Western blotting, immunostaining and siRNA knockdown approaches to investigate how amikacin influenced MDA-MB-231 cell migration and invasion. (3) Results: Wound healing showed that the MDA-MB-231 cell migration rates decreased to 44.4% in the presence of amikacin. Trans-well analysis showed that amikacin treatment led to invasion inhibition. Western blotting demonstrated that amikacin induced thioredoxin-interacting protein (TXNIP) up-regulation. TXNIP was knocked down using siRNA in MDA-MB-231 cell. Using immunostaining analysis, we found that inhibition of TXNIP expression led to MDA-MB-231 pseudopodia extension; however, amikacin treatment attenuated the cell extension formation. (4) Conclusions: We observed inhibition of migration and invasion in MDA-MB-231 cells treated with amikacin. This suggests inhibition might be mediated by up-regulation of TXNIP.
Insights
Amikacin antibiotic inhibits migration and invasion of human breast cancer cells (MDA-MB-231). This effect is linked to increased thioredoxin-interacting protein (TXNIP) levels, a key regulator of cell movement.
Area of Science:
- Oncology
- Cell Biology
- Pharmacology
Background:
- Amikacin is an aminoglycoside antibiotic crucial for treating gram-negative bacterial infections, particularly in immunocompromised cancer patients.
- Human breast cancer cells (MDA-MB-231) are aggressive and prone to metastasis, making them a relevant model for studying anti-migratory agents.
Purpose of the Study:
- To investigate the effects of amikacin on the migration and invasion capabilities of human MDA-MB-231 breast cancer cells.
- To elucidate the molecular mechanisms underlying amikacin's impact on cancer cell motility, focusing on the role of thioredoxin-interacting protein (TXNIP).
Main Methods:
- Utilized wound-healing and trans-well assays to quantify MDA-MB-231 cell migration and invasion rates.
- Employed Western blotting and immunostaining to analyze protein expression changes, specifically TXNIP and pseudopodia formation.
- Conducted siRNA knockdown experiments to assess the functional significance of TXNIP in amikacin-treated cells.
Main Results:
- Amikacin treatment significantly reduced MDA-MB-231 cell migration by 44.4% and inhibited cell invasion.
- Western blotting revealed that amikacin up-regulates the expression of thioredoxin-interacting protein (TXNIP).
- Knockdown of TXNIP using siRNA promoted pseudopodia extension, while amikacin treatment attenuated this effect, indicating TXNIP's role in mediating amikacin's anti-migratory action.
Conclusions:
- Amikacin effectively inhibits migration and invasion in MDA-MB-231 breast cancer cells.
- The observed anti-migratory and anti-invasive effects of amikacin are likely mediated through the up-regulation of TXNIP.
- These findings suggest a potential therapeutic role for amikacin beyond its antibacterial activity in managing breast cancer metastasis.
