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A comprehensive metabonomic and transcriptomic analysis reveals how inhibiting glycolysis affects regulatory T cell proliferation

ABSTRACT:

Background: Blocking glycolysis inhibits regulatory T cells (Tregs), which are often hijacked by tumor cells whose survival relies on glycolysis to inhibit antitumor immunity. However, how glycolysis influences Treg proliferation/differentiation remains unclear. Monocarboxylate transporters (MCTs) are key regulatory proteins that affect glycolysis.

Methods: To describe the potential mechanism underlying the effect of glycolysis on Treg proliferation and differentiation as well as the role of MCT1 on Treg metabolism, we conducted a comprehensive metabonomic and transcriptomic analysis using omics and molecular biology techniques.

Results: Fifteen differential metabolites and 2232 differentially expressed genes (DEGs) were identified, which were subjected to Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis to determine the most widely affected pathways. The results revealed that the adenosine triphosphate-binding cassette (ABC) transporter metabolism pathway was the most differentially activated between these two groups. According to The Cancer Genome Atlas (TCGA) database, the expression of ABC transporter-related genes affects renal clear cell carcinoma prognosis and is closely related to tumor immune cell infiltration.

Conclusions: The comprehensive analysis showed that MCT1-induced ABC transporter disorder has important effects on Treg biology. These insights will help to clarify the mechanism of MCT1-induced Treg growth inhibition and emphasize the importance of omics research for deepening the understanding of tumor cell proliferation mechanisms.

INSTRUMENT(S): Liquid Chromatography MS - positive - hilic, Liquid Chromatography MS - negative - hilic

SUBMITTER: Ziyu Wang

PROVIDER: MTBLS8002 | MetaboLights | 2024-08-06

REPOSITORIES: MetaboLights

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Project description:The ATP binding cassette (ABC) transporter family is widely distributed in vertebrates and is essential for drug resistance, cell signaling and energy homeostasis. There is growing evidence that various ABC transporters contribute to the growth and development of tumors but relatively little is known about how the ABC transporter family behaves in hepatocellular carcinoma (HCC). ABCC6 transporter was downregulated in HCC tissues and that it was associated with successful treatment for HCC patients. Cellular model studies have shown that ABCC6 plays a role in the migration and cytoskeleton rearrangement of HepG2 hepatocarcinoma cells, highlighting its role in cancer biology. Abcc6-silenced HepG2 cells are used as cell model to obtain more deep information about the molecular mechanisms underlying the observed results. MTT and colony formation assays, showed the effects of Abcc6 on HepG2 cell proliferation. Western blotting analysis, real-time PCR, and immunofluorescence were used to find the E-cadherin, Vimentin, and N-cadherin markers associated with the epithelial-to-mesenchymal transition (EMT). Colony formation experiments in the current study showed that Abcc6 decreased HepG2 cell viability. The migratory and invasion activities were dramatically slowed down by Abcc6 silencing, according to the Transwell and wound-healing assays. In tumor cells, EMT has been shown to be crucial for enhancing migration and invasion and is frequently characterized by a loss of epithelial markers (E-cadherin) and an increase in mesenchymal markers (Vimentin and N-cadherin). In the western blotting examination, E-cadherin expression was considerably elevated compared to the control group, while N-cadherin and Vimentin expression were downregulated. This led to the hypothesis that the underlying mechanism of Abcc6 knockdown prevents migration and invasion in HepG2 cells and is linked to the suppression of EMT. In conclusion all evidence suggested that ABC transporters play a more active role in cancer biology.

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A comprehensive metabonomic and transcriptomic analysis reveals how inhibiting glycolysis affects regulatory T cell proliferation

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