Similar Datasets
Project description:Using ATAC-seq, we identified differential chromatin accessibility comparing LSD1 wild type versus knockout GC B cells.
2018-12-13 | GSE119222 | GEO
Project description:Chromatin accessibility by ATAC in wild type versus knockout GC B cells
| PRJNA488487 | ENA
Project description:Many cancers rely on glycolytic metabolism to fuel rapid proliferation. This has spurred interest in designing drugs that target tumor glycolysis such as AZD3965, a small molecule inhibitor of Monocarboxylate Transporter 1 (MCT1) currently undergoing Phase I evaluation for cancer treatment. Since MCT1 mediates proton-linked transport of monocarboxylates such as lactate and pyruvate across the plasma membrane (Halestrap and Meredith, 2004), AZD3965 is thought to block tumor growth through disruption of lactate transport and glycolysis. Here we show that MCT1 inhibition impairs proliferation of glycolytic breast cancer cells that express MCT4 via disruption of pyruvate rather than lactate export. We found that MCT1 expression is elevated in glycolytic breast tumors and cell lines as well as in malignant breast and lung tissues. High MCT1 expression predicts poor prognosis in breast and lung cancer patients. Stable knockdown and AZD3965-mediated inhibition of MCT1 promote oxidative metabolism. Acute inhibition of MCT1 reduces pyruvate export rate but does not consistently alter lactate transport or glycolytic flux in breast cancer cells that also express MCT4. Despite the lack of glycolysis impairment, MCT1 loss-of-function decreases breast cancer cell proliferation and blocks growth of mammary fat pad xenograft tumors. Our data suggest that MCT1 expression is elevated in glycolytic cancers to promote pyruvate export, which when inhibited enhances oxidative metabolism and reduces proliferation. This study presents an alternative molecular consequence of MCT1 inhibitors that further supports their use as anti-cancer therapeutics. Since MCT1 levels are elevated in glycolytic and malignant breast tumors, we hypothesized that MCT1 may contribute to the Warburg effect metabolic phenotype. To test this hypothesis, we generated whole genome microarray data from breast cancer cell lines either a) expressing a short hairpin (sh)RNA-mediated stable knockdown of MCT1; or b) treated for 24 hours with an MCT1 inhibitor (AZD3965). Scramble shRNA or DMSO were used as controls, and all conditions were analzed in triplicate. The cell lines used â HS578T, SUM149PT, and SUM159PT â are among the most glycolytic in a panel of 31 breast cancer cell lines.
2016-03-08 | E-GEOD-76675 | biostudies-arrayexpress
Project description:Many cancers rely on glycolytic metabolism to fuel rapid proliferation. This has spurred interest in designing drugs that target tumor glycolysis such as AZD3965, a small molecule inhibitor of Monocarboxylate Transporter 1 (MCT1) currently undergoing Phase I evaluation for cancer treatment. Since MCT1 mediates proton-linked transport of monocarboxylates such as lactate and pyruvate across the plasma membrane (Halestrap and Meredith, 2004), AZD3965 is thought to block tumor growth through disruption of lactate transport and glycolysis. Here we show that MCT1 inhibition impairs proliferation of glycolytic breast cancer cells that express MCT4 via disruption of pyruvate rather than lactate export. We found that MCT1 expression is elevated in glycolytic breast tumors and cell lines as well as in malignant breast and lung tissues. High MCT1 expression predicts poor prognosis in breast and lung cancer patients. Stable knockdown and AZD3965-mediated inhibition of MCT1 promote oxidative metabolism. Acute inhibition of MCT1 reduces pyruvate export rate but does not consistently alter lactate transport or glycolytic flux in breast cancer cells that also express MCT4. Despite the lack of glycolysis impairment, MCT1 loss-of-function decreases breast cancer cell proliferation and blocks growth of mammary fat pad xenograft tumors. Our data suggest that MCT1 expression is elevated in glycolytic cancers to promote pyruvate export, which when inhibited enhances oxidative metabolism and reduces proliferation. This study presents an alternative molecular consequence of MCT1 inhibitors that further supports their use as anti-cancer therapeutics.
2016-03-08 | GSE76675 | GEO
Project description:MCT1 was deleted in Saccharomyces cerevisiae and gene expression was measured over a timecourse.
2020-06-02 | GSE151606 | GEO
Project description:Adipose tissue is an active producer of lactate. In obesity, the increased size of adipocytes is accompanied by an increase in lactate production in adipose tissue, caused by hypoxia in obese adipocytes. How lactate affects metabolism in adipocyte and insulin sensitivity remains unclear. Here we develop a mouse model of MCT1,coding by Slc16a1, specific deletion in adipose tissues, using the AP2 promoter to drive Cre expression. This MCT1 AKO mice develop more severe insulin resistance in obesity with 16 weeks high fat diet treatment, while few changes happen to lipid metabolism in adipose tissues. We used RNA-seq to analyze the gene expression patterns of eWAT of obese MCT1 AKO mice compared to WT, and found significant changes in innate immune signaling and adipocyte apoptosis that reflect systemic inflammation and insulin resistance.
2021-10-01 | GSE184760 | GEO
Project description:MCT1 deletion in Saccharomyces cerevisiae
| PRJNA636574 | ENA
Project description:Analysis of chromatin accessibility in primary GCTB samples with ATAC-seq
2020-08-31 | E-MTAB-9512 | biostudies-arrayexpress
Project description:E. Coli Nissle wild type versus knockout strain grown in M-9 media.
2019-01-31 | MSV000083387 | MassIVE
Project description:Using RNA-seq we identified the gene expression changes in MCT1-deficient B cells.
2023-11-22 | GSE247200 | GEO