Unknown,Transcriptomics,Genomics,Proteomics

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Lactate- and hypoxia-induced beta-glucan masking in responding and non-responding Candida albicans clinical isolates

ABSTRACT: RNA sequencing was performed on Candida albicans clinical isolates that display normal (isolates: 3560, 3605, 3609, 4108, 4259) or aberrant (isolates: 3534, 3544, 3621, 3636, 4036) beta-glucan masking in response to lactate and hypoxia. Each clinical isolate was grown to exponential phase in GYNB under normoxic conditions and then exposed for 5 h to: (a) 1% lactate; (b) 0% lactate control; (c) hypoxia; or (d) normoxic control. Three independent experiments were performed for each clinical isolate.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Candida albicans

SUBMITTER:

PROVIDER: E-MTAB-10986 | biostudies-arrayexpress |

SECONDARY ACCESSION(S): ERP132007

REPOSITORIES: biostudies-arrayexpress

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Project description:Lactic acidosis and hypoxia are two prominent tumor microenvironmental stresses that are both known to exert important influences on gene expression and phenotypes of cancer cells. But very little is known about the cross-talk and interaction between these two stresses. We performed gene expression analysis of MCF7 cells exposed to lactic acidosis, hypoxia and combined lactic acidosis and hypoxia. We found the hypoxia response elicited under hypoxia was mostly abolished upon simultaneous exposure to lactic acidosis. The repression effects are due to loss of HIF-1Î± protein synthesis under lactic acidosis. In addition, we showed lactic acidosis strongly synergizes with hypoxia to activate the unfold protein response (UPR) and inflammation response which are highly similar to amino acid deprivation responses (AAR). The statistical factor analysis of hypoxia and lactic acidosis responses indicated that ATF4 locus, an important activator in the UPR/AAR pathway, is amplified in subsets of breast tumors and cancer cell lines. Varying ATF4 levels dramatically affect the ability to survive the post-stress recovery from hypoxia and lactic acidosis and may suggest its selection of ATF4 amplification in human cancers. These data suggest that lactic acidosis interacts with hypoxia by both inhibiting the canonical hypoxia response and while activating the UPR and inflammation response. Gain of ATF4 locus may offer survival advantages to allow successful adaptation to frequent fluctuations of oxygen and acidity in tumor microenvironment. Collectively, our studies have provided linkage between the short-term transcriptional responses to the long term selection of the DNA copy number alterations (CNAs) under tumor microenvironmental stresses. RNAs from MCF7 cells exposed to control condition (ambient air ~21% O2, no lactate and neutral pH), lactic acidosis (ambient air, 10 mM Lactate and pH 6.7), hypoxia (1% pO2, no lactate and neutral pH) and the combined lactic acidosis and hypoxia (1% pO2, 10 mM Lactate and pH 6.7) condition for 24 hours were extracted by miRVana kits (Ambion) and hybridized to Affymetrix Human genome 133A 2.0 arrays with standard protocol.

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Lactate- and hypoxia-induced beta-glucan masking in responding and non-responding Candida albicans clinical isolates

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