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

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

PROVIDER: PRJNA633530 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11806608_1.fastq.gz	Fastqsanger.gz
	SRR11806608_2.fastq.gz	Fastqsanger.gz
	SRR11806609_1.fastq.gz	Fastqsanger.gz
	SRR11806609_2.fastq.gz	Fastqsanger.gz
	SRR11806610_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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.

2020-05-19 | GSE150761 | 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

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

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

| PRJNA1219396 | ENA

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

Bulk RNAseq in control and LACTB KO iPSC-derived microglia

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 the LACTB knock-out might lead to transcriptional changes in human induced pluripotent stem cells (iPSC)-microglia.

2026-08-05 | GSE323384 | GEO

Bulk RNAseq in control and LACTB KD human THP1 macrophages

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 the reduced levels of LACTB, using small-interfering RNA, might lead to transcriptional changes in human THP1 macrophages.

2026-08-05 | GSE323383 | GEO

Reduced LACTB expression in myeloid cells is associated with elevated succinyl-carnitine levels and reduced Alzheimer’s disease risk

Project description:Lactamase B (LACTB) is a mitochondrial protease previously related with cancer progression, and lipid metabolism. Our mendelian randomization analyses indicate that lower LACTB expression in myeloid cells is protective for Alzheimer’s Disease (AD) and is genetically associated with increased succinyl-carnitine, a poorly characterized metabolite that independently correlates with reduced AD risk. We identify LACTB as a primary enzyme responsible for succinyl-carnitine hydrolysis. Using human LACTB knockdown and knockout macrophage and microglial systems, we show that loss of LACTB enhances oxidative phosphorylation, reduces protein synthesis, and alters lipid profiles. LACTB expression is increased upon IFN/TNF stimulation, and LACTB loss modifies efferocytosis-related pathways following inflammatory activation. In vivo, xenotransplanted human LACTB knockout microglia show enhanced association with amyloid plaques in the mouse brain. Together, these findings define a previously unrecognized metabolic pathway linking LACTB and succinyl-carnitine to myeloid cell function and AD risk. Given its enzymatic druggability and the potential to leverage succinyl-carnitine as a translational biomarker, LACTB represents a promising therapeutic target.

2026-08-01 | GSE324494 | GEO

Targeted ErbB3 loss in mammary organoids harvested from ErbB3 DOX-KO mice +/- DOX treatment

2012-01-04 | GSE32129 | GEO

Targeted ErbB3 loss in mammary organoids harvested from ErbB3 DOX-KO mice +/- DOX treatment

Project description:Mammary organoids harvested from ErbB3 DOX-KO mice, which utilize MMTV-Cre transgene expression in the LE to cause genomic recombination at floxed ErbB3 alleles in ErbB3FL/FL were cultured in the presence or absence of doxycycline to induce ErbB3 loss. The gene expression shift following DOX-induced ErbB3 loss in the 3D organoids was examined by microarray. Gene expression patterns were interrogated in mammary organoids from ErbB3 inducible-knockout mice cultured in the presence of absence of doxycycline. Three biological replicates of the experiment were performed, resulting in a total of 6 samples (3 treatment, 3 control).

2012-01-04 | E-GEOD-32129 | biostudies-arrayexpress

Quantitative phosphoproteomics analysis of ERBB3/ERBB4 signaling

Project description:The four members of the epidermal growth factor receptor (EGFR/ERBB) family form homo- and heterodimers which mediate ligand-specific regulation of many key cellular processes in normal and cancer tissues. While signaling through the EGFR has been extensively studied on the molecular level, signal transduction through ERBB3/ERBB4 heterodimers is less well understood. Here, we generated isogenic mouse Ba/F3 cells that express full-length and functional membrane-integrated ERBB3 and ERBB4 or ERBB4 alone, to serve as a defined cellular model for biological and phosphoproteomics analysis of ERBB3/ERBB4 signaling. ERBB3 co-expression significantly enhanced Ba/F3 cell proliferation upon neuregulin-1 (NRG1) treatment. For comprehensive signaling studies we performed quantitative mass spectrometry (MS) experiments to compare the basal ERBB3/ERBB4 cell phosphoproteome to NRG1 treatment of ERBB3/ERBB4 and ERBB4 cells. We employed a workflow comprising differential isotope labeling with mTRAQ reagents followed by chromatographic peptide separation and final phosphopeptide enrichment prior to MS analysis. Overall, we identified 9686 phosphorylation sites which could be confidently localized to specific residues. Statistical analysis of three replicate experiments revealed 492 phosphorylation sites which were significantly changed in NRG1-treated ERBB3/ERBB4 cells. Bioinformatics data analysis recapitulated regulation of mitogen-activated protein kinase and Akt pathways, but also indicated signaling links to cytoskeletal functions and nuclear biology. Comparative assessment of NRG1-stimulated ERBB4 Ba/F3 cells indicated that ERBB3 did not trigger defined signaling pathways but more broadly enhanced phosphoproteome regulation in cells expressing both receptors. In conclusion, our data provide the first global picture of ERBB3/ERBB4 signaling and provide numerous potential starting points for further mechanistic studies

2016-01-15 | PXD002665 | Pride

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