Abstract
Abstract Mycoplasma are the smallest self-replicating prokaryotes and are burdened by their notoriety. It is widely unknown that mycoplasma are readily detected in many primary human cancer tissues and can influence tumorigenesis. Some mycoplasma species such as M. fermentans and M. hyorhinis can transform normal murine and human cell lines into tumorigenic cells. Mycoplasma infection can inactivate tumor suppressor genes and activate oncogenes. These observations suggest that mycoplasma can be both carcinogenic and or onco-modulators. We found that M. arginini was present in the metastatic macrophage cell line VM-M3 (referred to as M3myco+). Antibiotic was used to eradicate M. arginini (verified by mycoplasmal 16S rDNA PCR amplification) from the M3 cells (M3myco- cells). Oxygen consumption rate was higher in the than the M3myco- cells than in the M3myco+ cells, whereas lactate production was similar in both the M3myco+ and M3myco- cells. Glucose suppressed oxygen consumption in both cell lines indicating a Crabtree effect. The in-vitro proliferation rate was similar in both cell lines when seeded at low density, but was higher in the M3myco+ cells than in the M3myco- cells at higher cell densities. Tumor size at the primary inoculation site in flank was notably smaller and systemic metastasis in the syngeneic inbred VM mouse host was qualitatively less for the M3myco- cells than for the M3myco + cells, respectively. Survival was also longer in VM mice inoculated with the M3myco- cells compared to the M3myco+ cells. Our data indicate that M. arginini is an onco-modulator that might influence tumor growth through an effect tumor cell energy metabolism. (Supported by Boston College Research Expense fund). Citation Format: Roberto Flores, Ashley K. Brown, Zeynep Akgoc, Thomas N. Seyfried. Mycoplasma arginini infection shifts the energy catabolism ratio of metastatic macrophages towards fermentation and is associated with an increase in primary tumor size, metastasis and malignancy. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4318. doi:10.1158/1538-7445.AM2014-4318
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