Jilian Su1, Junmei Wang2, Jiamin Luo2, Haili Li2. 1. Department of the Second Ultrasonography, Women's Hospital, School of Medicine, Zhejiang University, China. Electronic address: 5506034@zju.edu.cn. 2. Department of the Second Ultrasonography, Women's Hospital, School of Medicine, Zhejiang University, China.
Abstract
AIMS: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
AIMS: 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 humanbreast cancer cells. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Authors: Simone A G Langeveld; Bram Meijlink; Inés Beekers; Mark Olthof; Antonius F W van der Steen; Nico de Jong; Klazina Kooiman Journal: Pharmaceutics Date: 2022-01-28 Impact factor: 6.321
Authors: Ali Jangjou; Amir Hossein Meisami; Kazem Jamali; Mohammad Hadi Niakan; Milad Abbasi; Mostafa Shafiee; Majid Salehi; Ahmad Hosseinzadeh; Ali Mohammad Amani; Ahmad Vaez Journal: J Biomed Sci Date: 2021-06-21 Impact factor: 8.410