Ultrasound-mediated destruction of vascular endothelial growth factor (VEGF) targeted and paclitaxel loaded microbubbles for inhibition of human breast cancer cell MCF-7 proliferation
Molecular and Cellular Probes, ISSN: 0890-8508, Vol: 46, Page: 101415
2019
- 14Citations
- 24Captures
- 2Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations14
- Citation Indexes14
- CrossRef14
- 14
- Captures24
- Readers24
- 24
- Mentions2
- References2
- Wikipedia2
Article Description
Vascular endothelial growth factor (VEGF) can promote cell division, proliferation and migration. In this study, we aimed to investigate roles of ultrasound-mediated destruction of VEGF-targeted and paclitaxel (PTX)-loaded lipid microbubbles (VTPLLM + US) in human breast cancer cells. The activity of MCF-7 cells was determined by cell counting Kit-8. Flow cytometry was performed to detect the cells apoptosis and cell cycle. The expression of cell cycle-associated proteins, matrix metalloprotein-9 (MMP-9), VEGF and apoptosis-associated proteins were detected by qRT-PCR and Western blot. The obtained data suggested that VTPLLM + US promoted the G1 phase cell cycle arrest and suppressed the viability of MCF-7 cells. We also found that VTPLLM + US accelerated cells apoptosis. Cell cycle-associated proteins and VEGF expression were modulated by VTPLLM + US. Moreover, VTPLLM + US was found to regulate the expression levels of apoptosis-associated proteins in MCF-7 cells. Our findings suggested that VTPLLM + US suppressed the proliferation and accelerated the apoptosis of MCF-7 cells through regulating VEGF expression. The potential effects of VTPLLM + US on apoptosis of MCF-7 cells suggest that applying VTPLLM + US might be an effective strategy in breast cancer therapies.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0890850819301306; http://dx.doi.org/10.1016/j.mcp.2019.06.005; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85068025440&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/31228519; https://linkinghub.elsevier.com/retrieve/pii/S0890850819301306; https://dx.doi.org/10.1016/j.mcp.2019.06.005
Elsevier BV
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