The present work evaluated the immunomodulatory effect of thalidomide (Thal) at different doses on tumor-associated macrophages (TAMs) using a mouse model of human breast cancer. Mice were inoculated with 4T1 cells in the left flank and treated with Thal once a day at concentrations of 50, 100, and 150mg/kg body weight from the 5th day until the 28th day of tumor inoculation. The tumors were sized, proliferation index and TAMs count were evaluated in primary tumors and metastatic lungs. In addition, the metastasis rate was evaluated in the lungs. Thal at 150mg/kg significantly decreased tumor growth, proliferation index, and TAMs infiltration in primary tumors. Conversely, a higher number of TAMs and lower proliferation index were observed in metastatic lungs in mice treated with 150mg/kg of Thal. Furthermore, Thal at 150mg/kg significantly decreased the metastatic nodules in the lungs. Our findings demonstrated that Thal treatment considerably decreased the primary tumor and lung metastasis in mice associated with different TAM infiltration effects in these sites.
Breast cancer is one of the deadliest cancers in the world. Effective metastasis of the primary tumor to the bone, brain, lungs, and other organs are the causes for morbidity of breast cancer patients. Therefore, there is a necessity to detect metastasis early for successful therapy. One approach for detecting metastases early is to identify ways in which metastatic breast cancers modify the blood by releasing particles from the cancer cells. Here we are testing the idea that metastatic breast cancer cells export particles that are different from nonmetastatic cells. To do so, we raised antibodies against particles exported from breast cancer cells. We then tested whether these antibodies could distinguish between low and high metastatic breast cancer cell lines, and breast cancer cells that have a propensity to metastasize to different organs. We found that antibodies detected CD81 and integrin alpha‐3 beta‐1 at much higher abundance in particles exported from low metastatic cells than high metastatic cells. This result supports the idea that CD81 and alpha‐3 beta‐1 integrin may be metastatic suppressors. In addition, we identified several other antibodies that bind differently to particles exported from the brain, bone, and lung specific organotropic breast cancer cells. Our findings suggest that particles exported from breast cancer cells change during metastatic progression, and raise the possibility that antibodies detecting such differences might be of prognostic value. Future work will identify the antigens for these antibodies, and test whether they can indeed distinguish organotropic metastases of breast cancer in blood plasma.
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