Tumor associated macrophages antagonize antitumor effect of chemotherapy.

2017 ◽  
Vol 35 (7_suppl) ◽  
pp. 120-120
Author(s):  
Fei Chen ◽  
Shicheng Su ◽  
Erwei Song

120 Background: Tumor associated macrophages play an essential role in tumor progression, promoting angiogenesis, immunosupression, invasion and metastasis. However, TAMs regulation of tumor responses to chemotherapy is complicated. In different type of treatment or tumor model, TAMs can either enhance or antagonize antitumor effect of chemotherapy. Methods: We isolated TAMs from breast cancer tissues, or PBMC stimulated with culture medium of mesenchymal breast cancer cells and cocultured with breast cancer cells MCF-7 for 6-10days. After cocultured with TAMs, we treated MCF-7 with docetaxel. In vivo, we use MCF-7 with or without TAMs to generate xenografts in NOD/SCID mice and treated with docetaxel. To testify if the antagonize was dependent on specific treatment, we also treated breast cancer cells with ciaplatin. Results: With coculture of TAMs, we obversed ruduced apoptosis of docetaxel treated breast cancer cells. In mice model, TAMs co-injection xenografts antagonized the antitumor effect of docetaxel.Consisted with previous results, TAMs coculture antagonize the antitumor effect of cisplatin, suggesting the antagonize of TAMs was independent on cell cycle. Conclusions: Collectively, our study indicated the antagonize of TAMs towards chemotherapy.

2012 ◽  
Vol 53 ◽  
pp. S119-S120
Author(s):  
A.S. Fernandes⁎ ◽  
M. Cipriano ◽  
J. Costa ◽  
M.F. Cabral ◽  
J. Miranda ◽  
...  

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Yike Wang ◽  
Lifeng Dong ◽  
Fang Wan ◽  
Fangfang Chen ◽  
Dianlei Liu ◽  
...  

AbstractThis study explored the role of MTDH in regulating the sensitivity of breast cancer cell lines to gemcitabine (Gem) and the potential miRNAs targeting MTDH. The expression of MTDH in cancer tissues and cells was detected by immunohistochemical staining or qRT-PCR. The target genes for MTDH were predicted by bioinformatics and further confirmed by dual-luciferase reporter assay and qRT-PCR. Cancer cells were transfected with siMTDH, MTDH, miR-9-3p inhibitor, or mimics and treated by Gem, then CCK-8, colony formation assay, tube formation assay, flow cytometry, wound healing assay, and Transwell were performed to explore the effects of MTDH, miR-9-3p, and Gem on cancer cell growth, apoptosis, migration, and invasion. Expressions of VEGF, p53, cleaved caspase-3, MMP-2, MMP-9, E-Cadherin, N-Cadherin, and Vimentin were determined by Western blot. MTDH was high-expressed in cancer tissues and cells, and the cells with high-expressed MTDH were less sensitive to Gem, while silencing MTDH expression significantly promoted the effect of Gem on inducing apoptosis, inhibiting cell migration, invasion, and growth, and on regulating protein expressions of cancer cells. Moreover, miR-9-3p had a targeted binding relationship with MTDH, and overexpressed miR-9-3p greatly promoted the toxic effects of Gem on cancer cells and expressions of apoptosis-related proteins, whereas overexpressed MTDH partially reversed such effects of overexpressed miR-9-3p. The study proved that miR-9-3p regulates biological functions, drug resistance, and the growth of Gem-treated breast cancer cells through targeting MTDH.


2019 ◽  
Vol 381 (2) ◽  
pp. 280-287
Author(s):  
Carla Fourie ◽  
Tanja Davis ◽  
Jurgen Kriel ◽  
Anna-Mart Engelbrecht

Surgery ◽  
2006 ◽  
Vol 140 (4) ◽  
pp. 607-615 ◽  
Author(s):  
Elizabeth A. Peralta ◽  
Melita L. Viegas ◽  
Somaja Louis ◽  
Deborah L. Engle ◽  
Gary L. Dunnington

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