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Warburg effect enhanced by AKR1B10 promotes acquired resistance to pemetrexed in lung cancer-derived brain metastasis

ABSTRACT: To investigate the function of AKR1B10 in the lung cancer brain metastasis cells, we established PC9-BrM3 cells in which AKR1B10 has been knocked down by shRNA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE211215 | GEO | 2023/08/23

REPOSITORIES: GEO

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CD146 as a potent target for anti-vascular therapies in lung cancer brain metastasis

Project description:To investigate the function of CD146 in the lung cancer brain metastasis cells, we established PC9-BrM3 cells in which CD146 has been knocked down by shRNA.

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Reactive astrocytes promote tumor progression via up-regulating tumor PCDH1 expression in lung cancer brain metastasis

Project description:To investigate the function of PCDH1 in the lung cancer brain metastasis cells, we established PC9-BrM3 cells in which PCDH1 has been knocked down by shRNA.

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Warburg effect enhanced by AKR1B10 promotes acquired resistance to pemetrexed in lung cancer-derived brain metastasis

Project description:Warburg effect enhanced by AKR1B10 promotes acquired resistance to pemetrexed in lung cancer-derived brain metastasis

2023-07-10 | PXD043632 |

Comparative transcriptome of cancer cells with enhanced brain tropism

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Warburg effect enhanced by AKR1B10 promotes acquired resistance to pemetrexed in lung cancer-derived brain metastasis

Project description:Warburg effect enhanced by AKR1B10 promotes acquired resistance to pemetrexed in lung cancer-derived brain metastasis

| PRJNA869568 | ENA

Warburg effect enhanced by AKR1B10 promotes acquired resistance to pemetrexed in lung cancer-derived brain metastasis.

Project description:BackgroundResistance to pemetrexed (PEM), a rare chemotherapeutic agent that can efficiently cross the blood-brain barrier, limits the therapeutic efficacy for patients with lung cancer brain metastasis (BM). Aldo-keto reductase family 1 B10 (AKR1B10) was recently found to be elevated in lung cancer BM. The link between AKR1B10 and BM-acquired PEM is unknown.MethodsPEM drug-sensitivity was assessed in the preclinical BM model of PC9 lung adenocarcinoma cells and the BM cells with or without AKR1B10 interference in vitro and in vivo. Metabolic reprogramming of BM attributed to AKR1B10 was identified by chromatography-mass spectrometry (GC-MS) metabolomics, and the mechanism of how AKR1B10 mediates PEM chemoresistance via a way of modified metabolism was revealed by RNA sequencing as well as further molecular biology experimental approaches.ResultsThe lung cancer brain metastatic subpopulation cells (PC9-BrM3) exhibited significant resistance to PEM and silencing AKR1B10 in PC9-BrM3 increased the PEM sensitivity in vitro and in vivo. Metabolic profiling revealed that AKR1B10 prominently facilitated the Warburg metabolism characterized by the overproduction of lactate. Glycolysis regulated by AKR1B10 is vital for the resistance to PEM. In mechanism, AKR1B10 promoted glycolysis by regulating the expression of lactate dehydrogenase (LDHA) and the increased lactate, acts as a precursor that stimulates histone lactylation (H4K12la), activated the transcription of CCNB1 and accelerated the DNA replication and cell cycle.ConclusionsOur finding demonstrates that AKR1B10/glycolysis/H4K12la/CCNB1 promotes acquired PEM chemoresistance in lung cancer BM, providing novel strategies to sensitize PEM response in the treatment of lung cancer patients suffering from BM.

| S-EPMC10428599 | biostudies-literature

Characterizing an HSF1-dependent transcriptional program in metastatic lung adenocarcinoma

Project description:The purpose of this study was to identify gene targets differentially regulated by shRNA-mediated knockdown of the HSF1 transcription factor in the brain-metastatic lung adenocarcinoma cell line PC9-BrM3.

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The effect on gene expression by p53 family members and the knockdown of AKR1B10

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Identification of PARP1 target genes using microarray

Project description:Purpose:To indentify downtream effectors of PARP1, we performed microarray profiling in non-targeting or PARP1 targeting shRNA-expressing H2030-BrM3. Results: we identifed 15 genes whose expression were decreased upon depletion of PARP1 in H2030-BrM3 cells at least by under 1.3-fold.

2015-10-07 | GSE73735 | GEO

The effect on gene expression by p53 family members and the knockdown of AKR1B10

Project description:To evaluate the effect on gene expression by p53 family members and AKR1B10, we overexpressed p53 family members in H1299 cells or knocked down AKR1B10 in HCT116 cells and evaluated the gene expression by microarray analysis. Gene expression was measured in H1299 cells infected with adenovirus expressing p53, p63g and p73b, and in HCT116 cells transfected with siRNAs targeting AKR1B10 and then treated with adriamycin.

2013-10-31 | E-GEOD-47096 | biostudies-arrayexpress

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