| 2014 |
In zebrafish, meox1 specifies endotomal endothelial precursor cells within a sub-compartment of the nascent somite (the endotome); these cells migrate to colonize the dorsal aorta and induce haematopoietic stem cell formation via chemokine signalling. Loss of meox1 expands the endotome at the expense of muscle precursors (external cell layer), generating excess endotome-derived cells in the dorsal aorta and a dramatic increase in HSC induction. |
Zebrafish loss-of-function genetics, lineage tracing, live imaging, epistasis with chemokine pathway mutants |
Nature |
High |
25119043
|
| 2017 |
Meox1 directly inhibits the cell-cycle checkpoint gene ccnb1 (cyclin B1), thereby initiating G2 cell-cycle arrest within muscle stem cells. Disrupting this G2 arrest causes premature lineage commitment and defects in muscle growth. This establishes a Meox1→ccnb1 repression axis governing muscle stem cell dynamics during zebrafish myotome growth. |
Zebrafish genetics, clonal analysis, chromatin binding assays (direct inhibition of ccnb1 promoter), rescue experiments with ccnb1 overexpression |
Cell stem cell |
High |
28686860
|
| 2009 |
Meox1 occupies conserved promoter regions of the transcription factor genes Tbx18 and Uncx (as well as the previously known target Bapx1) in the sclerotome, as shown by chromatin immunoprecipitation. Loss of Meox1 in mice alters relative cell proliferation rates in the rostral vs. caudal sclerotome, disrupts rostro-caudal polarity, and causes atlas-to-basioccipital assimilation—demonstrating a non-redundant role for Meox1 in maintaining sclerotome polarity through direct transcriptional regulation of downstream transcription factors. |
Mouse homozygous knockout, chromatin immunoprecipitation (ChIP) for conserved promoter elements, proliferation assays, gene expression analysis |
Developmental biology |
High |
19520072
|
| 2011 |
MEOX1 (and MEOX2) activate p16(INK4a) expression in a DNA-binding-dependent manner, whereas they induce p21(CIP1/WAF1) in a DNA-binding-independent manner, both leading to G1/S cell-cycle arrest and endothelial cell senescence. This demonstrates mechanistically distinct modes of transcriptional activation for two CDK inhibitor target genes. |
Overexpression of wild-type vs. DNA-binding-deficient MEOX1/MEOX2 mutants in vascular endothelial cells; cell cycle and senescence assays |
PloS one |
High |
22206000
|
| 2011 |
Meox1 is a direct transcriptional target of Hoxa2 in the second branchial arch: Hoxa2 binds two conserved sites in the Meox1 proximal promoter by ChIP, and these sites are required for Hoxa2-dependent Meox1 promoter activation. Furthermore, Meox1 protein can bind the same DNA sequences recognized by Hoxa2 on Hoxa2 target genes, placing Meox1 genetically downstream of Hoxa2 in branchial arch morphogenesis. |
ChIP (Hoxa2 on Meox1 promoter), promoter reporter assays with binding-site mutations, Meox1/Meox2 double-mutant mouse genetics, DNA-binding assays |
Molecular and cellular biology |
High |
21245383
|
| 2018 |
Meox1 transcriptionally activates Gata4 in cardiomyocytes, as demonstrated by promoter-activity assays and ChIP. Meox1 overexpression exacerbates pathological cardiac hypertrophy (familial and pressure-overload models), while knockdown ameliorates it; Gata4 knockdown abolishes these effects, placing Meox1 upstream of Gata4 in pathological hypertrophic remodelling. |
Cardiac-specific overexpression and knockdown (mouse models), digital gene expression profiling, promoter luciferase assay, ChIP, Gata4 knockdown rescue |
Cardiovascular research |
High |
29155983
|
| 2021 |
MEOX1 binds to the transcriptional initiation site of CCNB1 (cyclin B1) and suppresses its expression, causing G2-phase cell-cycle arrest and inhibiting NSCLC cell proliferation. CCNB1 overexpression rescues the growth inhibition caused by MEOX1 overexpression, establishing a MEOX1→CCNB1 repression axis in lung cancer cells. |
ChIP (MEOX1 on CCNB1 promoter), stable MEOX1 overexpression, in vitro/in vivo proliferation assays, CCNB1 rescue overexpression |
Environmental toxicology |
Medium |
34837450
|
| 2020 |
Combined p53- and PTEN-deficiency activates MEOX1 expression in TNBC cells. MEOX1 knockdown in these cells decreases expression of TYK2, STAT5B, and STAT6, abolishes cell proliferation in vitro, and inhibits tumor growth in vivo, indicating MEOX1 is required for growth downstream of combined p53/PTEN loss and upstream of JAK-STAT signalling components. |
siRNA double knockdown of p53 and PTEN, MEOX1 siRNA knockdown, RNA-Seq, immunoblotting, in vivo xenograft |
The Journal of biological chemistry |
Medium |
32467227
|
| 2020 |
TGF-β1 transcriptionally upregulates Meox1 in adult human dermal fibroblasts via Smad2 and Smad3, which directly bind the Meox1 promoter as shown by ChIP-qPCR. Meox1 overexpression promotes, and Meox1 knockdown reduces, fibroblast migration in scratch and Transwell assays. |
Transcriptome sequencing, RT-PCR, ChIP-qPCR (Smad2/3 on Meox1 promoter), Smad overexpression and siRNA knockdown, scratch/Transwell migration assays |
Zhonghua shao shang za zhi |
Medium |
32241049
|
| 2024 |
Ailanthone (AIL) suppresses MEOX1 expression by disrupting the interaction between the transcription factor JUN and the MEOX1 promoter, thereby blocking JUN-dependent MEOX1 activation. MEOX1 knockdown inhibits TGF-β1-induced fibroblast activation and endothelial-to-mesenchymal transition in vitro and ameliorates bleomycin-induced pulmonary fibrosis in vivo. |
High-throughput small-molecule screening, promoter-binding disruption assay, MEOX1 knockdown in fibroblasts and endothelial cells, bleomycin mouse model, in vitro fibroblast activation assays |
Acta pharmaceutica Sinica. B |
Medium |
39220862
|
| 2024 |
MEOX1 promotes myofibroblast apoptosis resistance in pulmonary fibrosis by transcriptionally upregulating RGS4 (G-protein signaling regulatory factor 4) in TGF-β1-induced myofibroblasts. MEOX1 silencing enhances myofibroblast apoptosis and attenuates fibrosis progression in bleomycin-treated mice. |
Bioinformatics target prediction, siRNA-mediated MEOX1 knockdown, in vitro TGF-β1-induced myofibroblast model, apoptosis assays, bleomycin mouse model |
Journal of cellular physiology |
Low |
39319990
|
| 2026 |
Meox1 transcriptionally activates Cthrc1 (collagen triple helix repeat containing 1) in cardiac fibroblasts, which promotes Smad2/3 phosphorylation and cardiac fibroblast-to-myofibroblast conversion. Meox1 knockdown attenuates cardiac fibrosis post-MI; Cthrc1 overexpression abolishes this cardioprotection, establishing a Meox1→Cthrc1→p-Smad2/3 signalling axis. |
Mouse MI model with Meox1 knockdown, primary cardiac fibroblast gain/loss-of-function, ChIP or promoter analysis for Cthrc1, Smad2/3 phosphorylation assays, Cthrc1 rescue overexpression in vivo and in vitro |
International journal of biological sciences |
Medium |
41362745
|
| 2025 |
MEOX1 directly binds the ABHD3 gene promoter to activate its transcription, thereby driving circABHD3 generation. circABHD3 promotes YTHDF2-dependent m6A-mediated degradation of YPEL3 mRNA, activating β-catenin signalling and exacerbating hepatic fibrosis through EMT and mitochondrial impairment. |
Luciferase reporter assay, ChIP (MEOX1 on ABHD3 promoter), methylated RNA immunoprecipitation (MeRIP), RIP and RNA pull-down for circABHD3-YTHDF2 interaction, in vivo CCl4/BDL fibrosis mouse models with knockdown |
PLoS genetics |
Medium |
40100806
|
| 2026 |
MEOX1 binds the TEAD2 promoter (at the -988 to -982 nt region) to activate TEAD2 transcription in hepatic stellate cells, stimulating Hippo signalling target transcription and promoting HSC activation and proliferation. Ligustilide binds the HOX domain of MEOX1 (confirmed by CETSA and SPR), inhibiting its function and alleviating hepatic fibrosis. |
ChIP, promoter deletion/mutation assays, CETSA, SPR, siRNA knockdown, in vivo CCl4 mouse model, LX-2 cell functional assays |
British journal of pharmacology |
Medium |
42116734
|
| 2023 |
MEOX1 is expressed specifically in CD4+ Treg cells at levels comparable to FOXP3, is upregulated by IL-2, and has a permissive epigenetic landscape exclusively in Tregs. MEOX1 knockdown profoundly alters downstream gene expression programs and impairs Treg suppressive capacity, identifying MEOX1 as a FOXP3-dependent Treg transcription factor. |
Transcriptomic dataset analysis (48 CD4+ T cell conditions), reverse network engineering, epigenetic analysis, IL-2 stimulation, siRNA knockdown with functional suppression assays |
Frontiers in immunology |
Medium |
37559728
|
| 2021 |
Meox1 regulates SDF-1α expression in vascular smooth muscle cells (VSMCs) via activation of CDC42, and promotes CXCR4 expression in Sca-1+ progenitor cells also through CDC42. Meox1 knockdown abolishes Sca-1+ progenitor cell accumulation and migration into the neointima after vascular injury, and CXCR4 inhibition similarly blocks these effects. |
Rat carotid balloon injury model, adenoviral shRNA-mediated Meox1 knockdown, CDC42 inhibitor (ZCL278), CXCR4 inhibitor (AMD3100), immunostaining for PCNA/Meox1, neointima quantification |
Stem cell research & therapy |
Low |
34233723
|
| 2025 |
TGF-β1 upregulates MEOX1 expression in lung fibroblasts through the NOX4-ROS-Smad pathway. Fibroblast-specific MEOX1 knockdown protects mice from bleomycin-induced pulmonary fibrosis and reduces CTGF expression. In vitro, MEOX1 knockdown abolishes TGF-β1-induced mitophagy deficiency by downregulating CTGF, thereby inhibiting fibroblast senescence and over-activation. |
RNA-seq, bleomycin mouse model with AAV-shMEOX1 (fibroblast-specific), NOX4/ROS pathway inhibition, in vitro lung fibroblast assays |
European journal of pharmacology |
Low |
40780596
|
| 2026 |
In glioblastoma cells, MEOX1 represses PAX1, thereby promoting tumor cell proliferation, migration, and invasion. PAX1 overexpression in GBM cells inhibits Treg differentiation from co-cultured CD4+ T cells, while PAX1 knockdown promotes it, linking the MEOX1→PAX1 repression axis to both intrinsic tumor aggressiveness and immunosuppression in the tumor microenvironment. |
GBM cell line gain/loss-of-function, functional proliferation/migration/invasion assays, co-culture CD4+ T cell Treg differentiation assays, PAX1 overexpression rescue |
Scientific reports |
Low |
41692908
|
| 2026 |
MEOX1 binds the SPHK1 (sphingosine kinase 1) promoter to activate S1P synthesis in ovarian cancer cells, driving a dual autocrine (S1PR3-dependent proliferation/migration) and paracrine (S1P/S1PR1-dependent reprogramming of fibroblasts to VEGF-C-secreting CAFs) program that promotes lymphangiogenesis and lymph node metastasis. SPHK1 inhibition blunts these phenotypes; S1P supplementation restores them. |
MEOX1 overexpression in vivo LNM model, spatial transcriptomics, immunostaining, promoter binding assay (MEOX1 on SPHK1 promoter), SPHK1 inhibitor and S1P rescue experiments, CAF-LEC co-culture, 113-patient cohort validation |
Advanced science |
Medium |
42107070
|
| 2025 |
MEOX1 promotes SERPINE1 transcription in hepatic stellate cells (HSCs), thereby activating HSCs and promoting MASH-related liver fibrosis. MEOX1 knockdown suppresses HSC activation, proliferation, and migration; SERPINE1 was identified as the critical downstream target by RNA-seq. |
RNA-seq in MEOX1-knockdown HSCs, in vitro HSC functional assays (activation, proliferation, migration), MASH mouse model, AlphaFold/PyMOL interaction prediction |
The International journal of biological markers |
Low |
40270091
|
| 2020 |
PPARα directly regulates MEOX1 expression in cardiomyocytes; PPARα gene delivery reduces cardiac dysfunction and mitochondria-dependent apoptosis in doxorubicin-treated mice, and these cardioprotective effects are abolished by MEOX1 knockdown, placing MEOX1 downstream of PPARα in this cardioprotective pathway. |
rAAV9-mediated PPARα delivery in mice, MEOX1 knockdown rescue, cardiac function (echocardiography), apoptosis assays |
Frontiers in pharmacology |
Low |
33132907
|