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Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation [si-nc/si-Suclg2]

ABSTRACT: Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation [si-nc/si-Suclg2]

PROVIDER: PRJNA908261 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22523164.fastq.gz	Fastqsanger.gz
	SRR22523165.fastq.gz	Fastqsanger.gz
	SRR22523166.fastq.gz	Fastqsanger.gz
	SRR22523167.fastq.gz	Fastqsanger.gz
	SRR22523168.fastq.gz	Fastqsanger.gz

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Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation [si-nc/si-Suclg2]

Project description:Purpose: mRNAs sequencing of the gene expression differences in diffDC transfected with si-nc or si-Suclg2, the goals of this study are to investigate the biological effect of the metabolic enzyme succinate-CoA ligase subunit beta Suclg2 in regulating regulatory DC differentiation and function.

2023-11-27 | GSE220055 | GEO

Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation

Project description:Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation

| PRJNA906581 | ENA

Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation

Project description:Purpose: mRNAs sequencing of the gene expression differences in maDC and diffDC, the goals of this study are to investigate the biological effect of the metabolic enzyme succinate-CoA ligase subunit beta Suclg2 in regulating regulatory DC differentiation and function.

2023-11-27 | GSE219010 | GEO

Bulk RNAseq in microglia from wild-type (WT) and Lactamase B (LACTB) enymatic dead (ED) mice (LACTB S162I).

Project description:Our mendelian randomization analysis showed that lower expression of LACTB in myeloid cells might be protective for Alzheimer's Disease. We evaluated how microglial cells from LACTB enzymatic dead mice show transcriptional changes.

2026-03-24 | GSE324607 | GEO

LACTB inhibits lipid synthesis to suppress glioma growth by promoting Hsc70-mediated ERBB3 degradation

Project description:Abnormal lipid metabolism is a hallmark of tumor and represents an anti-cancer strategy. β-lactamase like protein (LACTB) is a novel tumor suppressor, but the biological function and the involved mechanism in glioma remain unclear. Here, we show that LACTB overexpression suppresses glioma growth while LACTB knockdown shows the opposite effect. By RNA-sequencing and untargeted lipidomics analysis, we find that LACTB overexpression inhibits the lipid synthesis of glioma cells. Mechanistically, LACTB downregulates ERBB3 and inhibits PI3K/AKT/mTOR signaling, which restrains the lipogenesis of tumor cells. We further uncover that LACTB overexpression decreases the protein stability of ERBB3 by lysosomal degradation. LACTB promotes the interaction of ERBB3 and Hsc70 to facilitate ERBB3 degradation in lysosome. Finally, we show that targeting LACTB/ERBB3 axis significantly suppresses glioma growth in the mouse model. Therefore, our study reveals the antitumoral role of LACTB in glioma and the LACTB/ERBB3 axis represents a potential new therapeutic target for this tumor.

2026-02-05 | GSE288782 | GEO

SUCLG2 Regulates Mitochondrial Dysfunction through Succinylation in Lung Adenocarcinoma.

Project description: Not available

| S-EPMC10724390 | biostudies-literature

RNAseq comparison between ovarian cancer cells re-expressing LACTB and primary ovarian cells

Project description:Describing the LACTB tumor suppressor activity in ovarian cancer cells

2022-10-02 | E-MTAB-12053 | biostudies-arrayexpress

As an unfavorable prognostic factor, LACTB promotes metastasis of nasopharyngeal carcinoma via activation of ERBB3/EGFR-ERK signaling

Project description:Nasopharyngeal carcinoma (NPC) is a malignant tumor originating from the nasopharyngeal epithelium and has the highest metastatic rate among head and neck cancers, NPC metastasis has become the main cause of treatment failure. The molecular basis regulating NPC metastasis remains obscure. Here we discovered a gene named LACTB Highly expressed in NPC tissues and aimed to investigate its role and regulatory mechanism in the metastasis of NPC.LACTB was found to promote NPC cellular motility in vitro and metastasis in vivo via the activation of the ERBB3/EGFR-ERK pathway on a histone H3 depending manner. Also, the elevated expression of LACTB in the primary NPC correlated with patient poor survival, indicating LACTB as a potential prognostic predictor and an anti-metastasis therapeutic target.

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Genome-wide maps of histone H3 K79 succinylation in U251 cells.

Project description:We report the nuclear Gcn5/α-KGDH complex plays vital role in histone H3 K79 succinylation. By obtaining over 731 million reads from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of histone H3 K79 succinylation, Gcn5, and α-KGDH in U251 cells.

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Project description:The evolution of cancer cells from a drug-tolerant persister (DTP) state into stably resistant clones is a primary barrier to the long-term efficacy of targeted therapies. Through longitudinal transcriptomic profiling across melanoma, non-small cell lung cancer (NSCLC), and colorectal cancer models, we uncover a conserved, biphasic regulation of telomerase as a fundamental driver of this process. Combining targeted therapies with telomerase inhibition (genetic or pharmacological) in melanoma and NSCLC models suppressed DTP cell formation and resistance progression in vitro and in vivo. Mechanistic dissection via RNA-seq revealed SUCLG2 as a critical downstream effector of the telomerase inhibitor 6-thio-dG; SUCLG2 knockdown phenocopied combinatorial efficacy. Complementary ATAC-seq demonstrated 6-thio-dG–induced chromatin remodelling at the SUCLG2 locus, reducing accessibility to downregulate expression and thereby impeding DTP proliferation and resistance evolution. Collectively, we establish preemptive telomerase inhibition as a vulnerability-directed strategy to ablate adaptive resistance across malignancies.

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