Breast cancer colonization by accelerates tumor growth.

is a lipophilic yeast that occurs abundantly in breast tumors and that may contribute to a shortened overall survival of breast cancer (BRAC) patients, suggesting that the yeast may participate in the carcinogenesis of BRAC. However, the mechanisms involved in the -based acceleration of BRAC are unknown. Here, we show that can colonize mammary tissue in 7,12-dimethylbenz[a] anthracene-induced mice. The abundance of shortened the overall survival and increased the tumor incidence. Transcriptome data illustrated that IL-17A plays a key role in tumor growth due to colonization, and tumor-associated macrophage infiltration was elevated during colonization which triggers M2 polarization of macrophages via toll-like receptors 4/nuclear factor kappa-B (Nf-κB) signaling. Our results show that the expression of sphingosine kinase 1 (Sphk1) is increased in breast tumors after inoculation with . Moreover, we discovered that Sphk1-specific small interfering RNA blocked the formation of lipid droplets, which can effectively alleviate the expression of the signal transducer and activator of the transcription 3 (STAT3)/Nf-κB pathway. Taken together, our results demonstrate that could be a possible factor for the progression of BRAC. The mechanisms by which promotes BRAC development involve the IL-17A/macrophage axis. Meanwhile, Sphk1 overexpression was induced by infection, which also promoted the proliferation of MCF-7 cells.IMPORTANCELiterature has suggested that is associated with breast tumors; however, this association has not been confirmed. Here, we found that colonizes in breast fat pads leading to tumor growth. As a lipophilic yeast, the expression of sphingosine kinase 1 (Sphk1) was upregulated to promote tumor growth after colonization. Moreover, the IL-17A/macrophages axis plays a key role in mechanisms involved in the -induced breast cancer acceleration from the tumor immune microenvironment perspective.