Candida albicans drives colorectal cancer progression by inducing hypoxia signaling
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ABSTRACT:
PROVIDER: PRJNA1173542 | ENA |
REPOSITORIES: ENA
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Project description:Colorectal cancer (CRC) is the third leading cause of cancer-related mortality worldwide. Gut microbiota, including fungal species, are increasingly implicated in CRC progression, while the molecular mechanisms underlying host-fungal interactions in this context remain poorly understood. Here, we show that Candida albicans (C. albicans) activates pro-metastatic signaling pathways, MAPK and NF-κB, leading to upregulation of oncogenic transcription factors c-Jun and c-Myc. This cascade stabilizes and activates hypoxia-inducible factor 1α (HIF-1α), a central regulator of tumor metabolic reprogramming and angiogenesis, ultimately fostering a pro-tumorigenic microenvironment. Mechanistically, we identify candidalysin, a secreted peptide toxin of C. albicans, as a critical effector that engages epidermal growth factor receptor (EGFR) and toll-like receptor 2 (TLR2) in a species- and cancer cell type-dependent manner. These findings are further supported by patient-derived colonic organoids. Collectively, our study delineates a C. albicans-EGFR/TLR2-ERK/NF-κB-HIF-1α axis that promotes hypoxia-like responses in CRC, revealing a previously underappreciated role of fungal pathogens in shaping the tumor microenvironment and offering potential targets for therapeutic interventions.
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Project description:Recent studies have shown that the transcriptional landscape of the pleiomorphic fungus Candida albicans is highly dependent upon growth conditions. Here using a dual RNA-seq approach we identified 299 C. albicans and 72 Streptococcus gordonii genes that were either up- or down-regulated specifically as a result of co-culturing these human oral cavity microorganisms. Seventy five C. albicans genes involved in responses to chemical stimuli, regulation, homeostasis, protein modification and cell cycle were statistically (P ≤0.05) upregulated, while 36 genes mainly involved in transport and translation were down-regulated. Upregulation of filamentation-associated TEC1 and FGR42 genes, and of ALS1 adhesin gene, concurred with previous evidence that the C. albicans yeast to hypha transition is promoted by S. gordonii. Increased expression of genes required for arginine biosynthesis in C. albicans was potentially indicative of a novel oxidative stress response. The transcriptional response of S. gordonii to C. albicans was less dramatic, with only eight S. gordonii genes significantly (P ≤0.05) up-regulated ≥ twofold (glpK, rplO, celB, rplN, rplB, rpsE, ciaR, and gat). The expression patterns suggest that signals from S. gordonii cause a positive filamentation response in C. albicans, while S. gordonii appears to be transcriptionally less influenced by C. albicans. Five Samples; Sample 1 - Candida albicans cells grown in hypha inducing conditions for two hours; Sample 2 - Candida albicans cells grown in hypha-inducing conditions for two hours before co-culture with Streptococcus gordonii cells for one hour in a 2:1 rato; Sample 3 - Candida albicans cells grown in hypha-inducing conditions for two hours before culture in Streptococcus gordonii media for one hour; Sample 4 - Candida albicans cells grown in hypha inducing conditions for two hours, filtered to remove Candida albicans cells and media added to Streptococcus gordonii cells for one hour; Sample 5 - Streptococcus gordonii cells alone for one hour. All samples extracted and sequenced in biological triplicate using Illumina HiSeq2500. Samples 1, 2 and 3 aligned to the reference genome for Candida albicans and Samples 2, 4 and 5 aligned to the reference genome for Streptococcus gordonii.
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