Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Wenshen Xiaozheng Tang ameliorates endometriosis by interrupting the lactate/H3K9la-mediated crosstalk between ectopic endometrial stromal cells and macrophages

ABSTRACT: WXT significantly reduced ectopic lesion volume, alleviated peritoneal adhesions, and decreased the proportion of M2 macrophages in both lesion tissues and peritoneal fluid, along with reduced lactate accumulation and suppressed M2-associated cytokine secretion. Single-cell transcriptomic analysis revealed enhanced glycolytic activity in eESCs and a positive correlation between M2 macrophage polarization and lactate-sensing gene signatures. WXT-containing serum inhibited eESC-derived lactate production, reduced H3K9la levels in macrophages, and blocked lactate-induced M2 polarization. Through UPLC-Q-TOF-MS/MS and molecular docking screening, we identified tormentic acid as a key absorbed component with strong predicted binding to both GLUT1 (a key glycolytic transporter) and p300 (a key regulator of histone lactylation). Tormentic acid reproduced the effects of WXT-containing serum, suppressing lactate production, reducing H3K9la levels, and attenuating M2 polarization. CUT&Tag and ChIP-qPCR further revealed that tormentic acid reduced H3K9la enrichment at the WNT2B promoter and suppressed its expression, defining a lactate-H3K9la-WNT2B axis through which tormentic acid ameliorates endometriosis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE342486 | GEO | 2026/08/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

UPF1-dependent glycolysis driven by LINC00887 facilitates macrophage M2 polarization in clear cell renal cell carcinoma

Project description:Clear cell renal cell carcinoma (ccRCC), a frequent urinary system tumor, is known for its poor patient outcomes. Here, we demonstrate that LINC00887 overexpression in ccRCC drives M2 macrophage polarization via aerobic glycolysis activation and lactate accumulation. Mechanistically, LINC00887 interacted with UPF1, leading to reduced UPF1 levels. UPF1, which is low in ccRCC, restrained cell vitality, proliferation, migration, invasion, and cell cycle progression in ccRCC cells, and stimulated apoptosis. Additionally, UPF1 was found to be negatively correlated with aerobic glycolysis in ccRCC, repressing glycolytic activity and M2 macrophage polarization while bolstering the tumor-killing potential of CD8+ T cells. By combining bioinformatics with experimental data from ccRCC single-cell RNA sequencing, we've demonstrated that reduced UPF1 expression can reprogram glycolytic metabolism, leading to an improved immunosuppressive tumor microenvironment.

2025-10-01 | GSE301681 | GEO

CUT - Tag detection results for H3K9la, H4K8la, and H4K16la in tenocyte

Project description:We found that lactate and lactylation were significantly elevated in rotator cuff tears, and lactylation primarily regulates histones in tenocytes. Therefore, we screened for histone lactylation and identified that H3K9, H4K8, and H4K16 had the most prominent increases. Subsequently, we conducted CUT - Tag assays on them. The results indicated that H3K9la was enriched at the promoters of ENO3 and COL1, while H4K16la was enriched at the promoter of TNMD, which induced the transcriptional expression of these genes. Moreover, as a glycolytic enzyme, ENO3 is further involved in the H3K9la–Eno3–lactate–H3K9la positive feedback loop to maintain a high lactate level. This feedback loop continuously drives the H3K9 - COL1 and H4K16 - TNMD regulatory axes, ultimately promoting the repair of rotator cuff tear injuries.

2025-09-30 | GSE309143 | GEO

Metabolic regulation of gene expression by histone lactylation

Project description:Cancer-augmented lactogenesis has been described by the Warburg effect, and is associated with several major hallmarks of neoplasia. However, the non-metabolic functions of elevated lactate in physiology and disease remain unknown. Here we report histone lysine lactylation as a new type of epigenetic mechanism and as a functional destination for lactate. Histone lactylation is induced under glycolytic conditions such as hypoxia and M1 macrophage polarization. In the late phase of M1 macrophage polarization, increases in histone lactylation but not acetylation mark M2-like genes for activation. Our findings suggest a feedback mechanism of the innate immune system to switch from proinflammation to resolution through histone Kla-associated gene expression. This mechanism is implemented by the coopted function of lactate and histone lactylation in metabolism and epigenetics. Together, our study opens a new avenue for understanding function of lactate and glycolysis underlined diverse pathophysiological conditions.

2019-08-06 | GSE115354 | GEO

AF9/KLF2 gene regulatory circuit links histone lactylation to breast cancer metastasis [RNA-seq]

Project description:Histone lysine L-lactylation (hereafter referred to as histone Kla) is a novel epigenetic mark induced by glycolytic metabolism, serving as a link between metabolic reprogramming and epigenetic regulation. In this study, we uncover an epigenetic-genetic transcriptional regulatory circuit involving AF9 and KLF2 that drives luminal breast cancer progression. AF9, identified as a reader of histone H3 lysine 9 lactylation (H3K9la), promotes KLF2 expression, while KLF2, functioning as a transcription factor for AF9, forms a positive feedback loop that amplifies lactylation-dependent effects. This circuit activates tumor-associated pathways, including TGFβ1, glucose and lactate transporters, and metabolic enzymes essential for glycolysis and serine biosynthesis, driving tumorigenesis and metastasis. Spatial and single-cell transcriptomics show AF9-positive tumor cells enriched in regions of active lactylation, correlated with immune evasion through interactions with M2 macrophages. Together, AF9, H3K9la, and KLF2 integrate metabolism, epigenetics, and signaling to promote tumor growth and metastasis, highlighting AF9's central role as a histone lactylation reader and a potential therapeutic target in breast cancer.

2026-03-03 | GSE291225 | GEO

AF9/KLF2 gene regulatory circuit links histone lactylation to breast cancer metastasis [CUT&Tag]

2026-03-03 | GSE291224 | GEO

Project description:The effect of lactate to M2-macrophage polarization

| PRJNA784245 | ENA

Hypoxia promotes histone H3K9 lactylation to enhance LAMC2 transcription in esophageal squamous cell carcinoma

Project description:Hypoxia promotes tumorigenesis and lactate accumulation in esophageal squamous cell carcinoma (ESCC). Lactate can induce histone lysine lactylation (Kla, a recently-identified histone marks) to regulate transcription. However, the functional consequence of histone Kla under hypoxia in ESCC remains to be explored. Here, we reveal that hypoxia facilitates histone H3K9la to enhance LAMC2 transcription for proliferation of ESCC. We found that global level of Kla was elevated under hypoxia, and thus identified the landscape of histone Kla in ESCC by quantitative proteomics. Furthermore, we show a significant increase of H3K9la level induced by hypoxia. Next, MNseq ChIP-seq and RNA-seq analysis suggest that H3K9la is enriched at the promoter of cell junction genes. Finally, we demonstrate that the histone H3K9la facilitates the expression of LAMC2 for ESCC invasion by in vivo and in vitro experiments. Briefly, our study reveal a vital role of histone Kla triggered by hypoxia in cancer.

2024-05-22 | GSE255352 | GEO

SIRT3 functions as an eraser of histone H3K9 lactylation to modulate transcription for inhibiting the progression of esophageal cancer

Project description:As a novel post-translational modification of histone derived from lactate, lysine lactylation (Kla) links lactate metabolism to epigenetic regulation, playing a role in modulation of gene expression in tumor and immune microenvironment. Evidence so far indicates that HDAC1-3 can catalyze the removal of Kla. However, the regulated targets of HDACs for Kla and functional consequence remain elusive. Herein, we used an antibody-based proximity labeling approach to identify SIRT3 binding to histone H3K9la and catalytic removal of the lactylationoup. The molecular docking results further revealed the mechanism of the binding of Kla peptide to SIRT3. More importantly, SIRT3 can specifically modulate the gene transcription by regulating H3K9la, inhibiting the progression of esophageal cancer cells (ESCC). In conclusion, our work identifies the delactylase of H3K9la and reveal an H3K9la-mediated molecular mechanism catalyzed by SIRT3 for gene transcription regulation in ESCC, and our findings provide an opportunity to investigate the physiological significance of Kla and shed light on the unknown cellular mechanisms controlled by SIRT3.

2025-02-24 | PXD054857 | Pride

Identification of SIRT3 as an eraser for H3K9 lactylation by antibody-mediated proximity labeling strategy

2024-08-18 | GSE274648 | GEO

Transcriptional profiling of THP-1 monocytes conditioned with Lacticaseibacilli rhamnosus R0011 secretome

Project description:Macrophage responses to activation are fluid and dynamic in their ability to respond appropriately to challenges, a role integral to host defence. While bacteria can influence macrophage differentiation and polarization into pro-inflammatory and alternatively activated phenotypes through direct interactions, many questions surround indirect communication mechanisms mediated through secretomes derived from gut bacteria, such as lactobacilli. We examined effects of secretome-mediated conditioning on THP-1 human monocytes, focusing on the ability of the Lacticaseibacillus rhamnosus R0011 secretome (LrS) to drive macrophage differentiation and polarization and prime immune responses to subsequent challenge with lipopolysaccharide (LPS). Genome-wide transcriptional profiling revealed increased M2-associated gene transcription in response to LrS conditioning in THP-1 cells. Cytokine and chemokine profiling confirmed these results, indicating increased M2-associated chemokine and cytokine production (IL-1Ra, IL-10). These cells had increased cell-surface marker expression of CD11b, CD86, and CX3CR1, coupled with reduced expression of the M1 macrophage-associated marker CD64. Mitochondrial substrate utilization assays indicated diminished reliance on glycolytic substrates, coupled with increased utilization of citric acid cycle intermediates, characteristics of functional M2 activity. LPS challenge of LrS-conditioned THP-1s revealed heightened responsiveness, indicative of innate immune priming. Resting stage THP-1 macrophages co-conditioned with LrS and retinoic acid also displayed an immunoregulatory phenotype with expression of CD83, CD11c and CD103 and production of regulatory cytokines. Secretome-mediated conditioning of macrophages into an immunoregulatory phenotype is an uncharacterized and potentially important route through which lactic acid bacteria and the gut microbiota may train and shape innate immunity at the gut-mucosal interface.

2024-04-12 | GSE225273 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data