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Mitochondrial dicarboxylate carrier SLC25A10 promotes HCC cell resistance to apoptosis by upregulating BCL2A1 expression [ChIP-seq]

ABSTRACT: This investigation delved into the role of the mitochondrial dicarboxylate carrier SLC25A10 in hepatocellular carcinoma's (HCC) resistance to chemotherapy. Herein, we disclosed the indispensable role of SLC25A10 in facilitating HCC's resistance to etoposide both in vitro and in mouse models. Hypoxia augmented SLC25A10 expression and instigated a splicing variation in SLC25A10 from isoform 1 to isoform 3. The isoform 3 of SLC25A10 translocated into the nucleus by associating with the nuclear transporter IPO7 and bound to the transcription factor CEBPB to upregulate the BCL2A1 expression, thereby escalating the HCC cell's resistance to Etoposide.

ORGANISM(S): Homo sapiens

PROVIDER: GSE279928 | GEO | 2025/10/16

REPOSITORIES: GEO

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Mitochondrial dicarboxylate carrier SLC25A10 promotes HCC cell resistance to apoptosis by upregulating BCL2A1 expression [RNA-seq]

Project description:This investigation delved into the role of the mitochondrial dicarboxylate carrier SLC25A10 in hepatocellular carcinoma's (HCC) resistance to chemotherapy. Herein, we disclosed the indispensable role of SLC25A10 in facilitating HCC's resistance to etoposide both in vitro and in mouse models. Hypoxia augmented SLC25A10 expression and instigated a splicing variation in SLC25A10 from isoform 1 to isoform 3. The isoform 3 of SLC25A10 translocated into the nucleus by associating with the nuclear transporter IPO7 and bound to the transcription factor CEBPB to upregulate the BCL2A1 expression, thereby escalating the HCC cell's resistance to Etoposide.

2025-10-16 | GSE279929 | GEO

Mitochondrial dicarboxylate carrier SLC25A10 promotes HCC cell resistance to apoptosis by upregulating BCL2A1 expression [RNA-seq]

Project description:Mitochondrial dicarboxylate carrier SLC25A10 promotes HCC cell resistance to apoptosis by upregulating BCL2A1 expression [RNA-seq]

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Mitochondrial dicarboxylate carrier SLC25A10 promotes HCC cell resistance to apoptosis by upregulating BCL2A1 expression [ChIP-seq]

Project description:Mitochondrial dicarboxylate carrier SLC25A10 promotes HCC cell resistance to apoptosis by upregulating BCL2A1 expression [ChIP-seq]

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The mitochondrial carrier SLC25A10 regulates cancer cell growth.

Project description:Dysregulation of cell metabolism is critical for the growth properties of cancer cells. The purpose of this study was to understand the role of substrate transport across the mitochondrial membrane to sustain the metabolic shift and redox defense in cancer cells. Mitochondrial carrier SLC25A10 is up-regulated in a variety of tumors and is involved in regulating intracellular levels of reactive oxygen species. We show that knockdown of SLC25A10 in A549 cells changed the growth properties to a less malignant phenotype and casued increased glutamine dependency and sensitivity to oxidative stress. The metabolic alteration was linked to an energy metabolic shift from glycolysis to mitochondrial oxidative phosphorylation illustrated by increased expression of glutamate dehydrogenase, decreased expression of lactate dehydrogenase due to down-regulation of hypoxia inducible factor 1?. We identified effects on NADPH production linked to the growth changes observed in SLC25A10 knockdown cells, demonstrated by decreased NADPH production in cells deprived of glutamine. The contribution of SLC25A10 to reprogram cell metabolism and to regulate cell growth suggests SLC25A10 as a novel target for anti-cancer strategies.

| S-EPMC4496216 | biostudies-literature

CRISPR/Cas9 Genome Editing of the Human Topoisomerase IIα Intron-19 5′ Splice Site Circumvents Etoposide Resistance in Human Leukemia K562 Cells

Project description:Results indicate that CRISPR/Cas9 gene editing of a suboptimal E19/I19 5′ splice site in the TOP2α gene results in circumvention of acquired drug resistance to etoposide and other TOP2-targeted drugs in a clonal K562 cell line by enhancing removal of intron 19 thereby decreasing formation of a truncated TOP2α/90 isoform and increasing expression of full-length TOP2α/170 in these resistant cells.

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SRSF7-mediated Alternative Splicing of USO1 Promotes Hepatocellular Carcinoma by Activating the MAPK/ERK1-ELK1 Pathway

Project description:We conducted a transcriptome-wide survey to identify novel hepatocellular carcinoma (HCC)-associated genes that have undergone aberrant alternative splicing. We revealed that the vesicle transport factor (USO1) is a major alternatively spliced target in HCC, mainly composed of a long wild-type isoform (USO1-L) and a short truncated isoform lacking exons 5 and 15 (USO1-S). A markedly increased isoform switching from USO1-L to USO1-S occurs in approximately 80% of HCCs and predicts poor clinical outcomes. USO1-L suppresses HCC cells growth and metastasis through weakening the activation of MAPK/ERK1-ELK1 signaling by interacting with phosphorylated ERK1 and anchoring it onto the Golgi apparatus to reduce its nuclear translocation; while USO1-S confers a loss-of-function effect. The splicing factor SRSF7, which is shown to be hypomethylated and upregulated in HCC, mediates the splicing of USO1-L to produce USO1-S. Notably, the loss of USO1-L in HCC cells induces their resistance to MEK inhibitors; however, restoring USO1-L through antisense oligodeoxynucleotide (ASO)-mediated blockade of switching from USO1-L to USO1-S can reverse this resistance. In summary, our findings highlight the crucial role of aberrantly alternative splicing of USO1 in HCC, as well as the SRSF7-USO1-MAPK axis as a potential target for this malignancy.

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2020-12-01 | GSE162322 | GEO

Mutant p53 cooperates with ETS2 to promote etoposide resistance

Project description:This SuperSeries is composed of the following subset Series: GSE36749: Mutant p53 cooperates with ETS2 to promote etoposide resistance [ChIP-Seq] GSE36751: Mutant p53 cooperates with ETS2 to promote etoposide resistance [ChIP-chip] Refer to individual Series

2012-05-02 | E-GEOD-36752 | biostudies-arrayexpress

Deciphering the Cancer Cell Resistome: Gene and microRNA Expression Signatures reveal Unique Molecular Targets for Therapeutic Intervention in Etoposide Resistant Breast Cancer

Project description:The second leading cause of cancer death for women in the U.S. is breast cancer. Moreover, a significant number of patients with breast tumors acquire resistance to drugs during therapy. To develop targeted therapeutic strategies to combat drug resistance it is essential to understand the basic molecular mechanisms through which cancer cells control sensitivity to chemotherapeutics. To identify new candidate genes and facilitate the discovery of novel drug resistance pathways, we have generated a resistance profile or ?resistome? of etoposide resistant MCF7 breast cancer cells. Differential expression of over 5000 genes (fold change > 2, P value < 0.05) indicate that several drug resistance mechanisms may be operating in these cells, including up-regulation of ABC transporter genes, down-regulation of the drug target and down-regulation of apoptotic genes. Several transcription factors such as RUNX2, SOX9, ETS1 and SMAD3 were up-regulated in the drug resistant cells. Targeted RUNX2 knockdown in the resistant cells using siRNA increased sensitivity to etoposide and also upregulated expression of pro-apoptotic genes indicating that RUNX2 could be a molecular target against etoposide resistance. Differential miRNA (microRNA) expression was observed among the drug resistant and sensitive cells suggesting that miRNA may also play a role in regulation of drug resistance. Hsa-miR-218, which targets ABCC6, was down-regulated in the drug resistant cell line. Transfection of a miR-218 mimic could down-regulate the expression of the efflux pump ABCC6 by 65% in drug resistant cells suggesting that regulation of miRNA may play an important role in etoposide resistance. long summary Refer to individual Series. This SuperSeries is composed of the following subset Series: GSE28413: Expression profile of etoposide-resistant MCF7 (MCF7VP) cells GSE28414: Expression profile of etoposide-resistant MCF7 (MCF7VP) cells with targeted RUNX2 knockdown

2011-04-08 | E-GEOD-28415 | biostudies-arrayexpress

Expression profile of etoposide-resistant MCF7 (MCF7VP) cells with targeted RUNX2 knockdown

Project description:The second leading cause of cancer death for women in the U.S. is breast cancer, moreover, a significant number of patients with breast tumors acquire resistance to drugs during therapy. To develop targeted therapeutic strategies to combat drug resistance it is essential to understand the basic molecular mechanisms through which cancer cells control sensitivity to chemotherapeutics. To identify new candidate genes and facilitate the discovery of novel drug resistance pathways, we have generated a resistance profile or M-bM-^@M-^XresistomeM-bM-^@M-^Y of etoposide resitant MCF7 breast cancer cells. Differential expression of over 5000 genes (fold change > 2, P value < 0.05) indicate that several drug resistance mechanisms may be operating in these cells, including up-regulation of ABC transporter genes, down-regulation of the drug target and down-regulation of apoptotic genes. Several transcription factors such as RUNX2, SOX9, ETS1 and SMAD3 were up-regulated in the drug resistant cells. Targeted RUNX2 knockdown in the resistant cells using siRNA increased sensitivity to etoposide and also upregulated expression of pro-apoptotic genes indicating that RUNX2 could be a molecular target against etoposide resistance. Differential miRNA (microRNA) expression was observed among the drug resistant and sensitive cells suggesting that miRNA may also play a role in regulation of drug resistance. Hsa-miR-218, which targets ABCC6, was down-regulated in the drug resistant cell line. Transfection of a miR-218 mimic could down-regulate the expression of the efflux pump ABCC6 by 65% in drug resistant cells suggesting that regulation of miRNA may play an important role in etoposide resistance. RNA from etoposide-resistant MCF7 (MCF7VP) cell lines were hybridized to Affymetrix microarrays.

2011-04-08 | E-GEOD-28414 | biostudies-arrayexpress

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