| 1997 |
Enforced expression of MCAM/MUC18 in MCAM-negative primary cutaneous melanoma SB-2 cells increased homotypic adhesion, attachment to human endothelial cells, and invasiveness through Matrigel; anti-MCAM monoclonal antibody reversed these functions, establishing a direct functional role for MCAM in tumor cell adhesion and invasion. |
cDNA transfection in melanoma cells, homotypic adhesion assay, endothelial attachment assay, Matrigel invasion assay, antibody blocking, in vivo tumorigenicity/metastasis in nude mice |
Cancer research |
High |
9187135
|
| 1997 |
MCAM mediates homotypic cell adhesion through interaction with a heterophilic (non-MCAM) ligand in a divalent-cation-independent, temperature-sensitive manner; homophilic MCAM-MCAM interactions were not supported by mixed aggregation assays with MCAM-expressing and non-expressing cells. |
cDNA transfection of MCAM-negative melanoma lines, homotypic aggregation assay, mixed aggregation assay, glycosaminoglycan inhibition assay |
International journal of cancer |
Medium |
9398060
|
| 1998 |
The transcription factor AP-2 directly binds to four AP-2 binding sites in the MCAM/MUC18 promoter and represses MCAM expression; loss of AP-2 in metastatic melanoma cells correlates with MCAM upregulation, and re-expression of AP-2 downregulates MCAM mRNA and protein. |
EMSA (electrophoretic mobility shift assay), promoter-reporter (CAT) assay with AP-2 transfection, AP-2 dose-dependent repression assay, Western blot, in vivo tumorigenicity in nude mice |
The Journal of biological chemistry |
High |
9632718
|
| 1996 |
Cyclic AMP elevation upregulates cell-surface MCAM/MUC18 expression and mRNA levels, while phorbol ester treatment downregulates both, demonstrating that MCAM expression is regulated by PKC and cAMP signaling pathways. |
cAMP analogue and phorbol ester treatment, flow cytometry for surface expression, Northern blot for mRNA quantification |
Cancer research |
Medium |
8616875
|
| 2000 |
The minimal MCAM promoter (-106/+22 bp) contains Sp-1 sites, AP-2 elements, and a CRE element; site-directed mutagenesis showed the CRE is a major transcriptional activator, while the AP-2 site at -23 bp has an inhibitory influence in AP-2-expressing cells, and AP-2 sites at -131 and -302 bp are activating. |
Deletion and site-directed mutagenesis of the MCAM promoter, promoter-reporter assay in melanoma/glioma/carcinoma cell lines |
The Journal of biological chemistry |
Medium |
10938273
|
| 2003 |
MelCAM/MCAM and AKT engage in reciprocal regulation in melanoma: pharmacological or dominant-negative inhibition of AKT reduces MelCAM expression, while overexpression of constitutively active AKT upregulates MelCAM; conversely, MelCAM overexpression activates endogenous AKT and inhibits pro-apoptotic BAD, increasing cell survival. |
Pharmacological AKT inhibition, constitutively active AKT overexpression, dominant-negative PI3K expression, Western blot for MelCAM/AKT/BAD, cell survival assay under stress |
Oncogene |
Medium |
14534536
|
| 2007 |
The long cytoplasmic isoform MCAM-l (but not MCAM-s) promotes microvilli formation and enhances lymphocyte rolling and adhesion to endothelial monolayers and VCAM-1; mutagenesis identified serine 32 in the MCAM-l cytoplasmic tail (a putative PKC phosphorylation site) as required for MCAM-l–actin cytoskeleton interaction and microvilli induction; PKC inhibition abolished these effects. |
Isoform transfection into NK cell line NKL1, shear-stress adhesion assay, scanning electron microscopy, site-directed mutagenesis (S32), PKC inhibitor treatment (chelerythrine chloride), anti-MCAM antibody blockade |
Journal of immunology |
High |
17982057
|
| 2006 |
The long isoform MCAM-l is targeted to the basolateral membrane of polarized MDCK epithelial cells, while MCAM-s is targeted to the apical membrane; a single dileucine motif (positions 41-42) in the MCAM-l cytoplasmic domain is required for basolateral targeting. |
Transfection of MCAM isoform–GFP chimeras in polarized MDCK cells, confocal microscopy, site-directed mutagenesis of the dileucine motif |
FEBS letters |
High |
16756976
|
| 2001 |
HEMCAM/CD146 expression in fibroblasts downregulates cell-surface levels of laminin-binding integrins α3β1, α6β1, α7β1, and fibronectin receptor α5β1; this downregulation occurs at a translational or post-translational level rather than at the transcriptional level, and both isoforms (HEMCAM-s and HEMCAM-l) inhibit integrin-dependent adhesion to laminin-1. |
Stable transfection of murine fibroblasts with HEMCAM isoforms, flow cytometry for integrin surface levels, immunoprecipitation, semi-quantitative PCR, Northern blot, cell adhesion/spreading assays |
Journal of cell science |
High |
11329371
|
| 2012 |
MCAM (CD146) is identified as a receptor for laminin-411 (an isoform of laminin expressed in vascular endothelial basement membranes); purified MCAM-Fc binds laminin-411 with an affinity of 27 nM; MCAM binding was undetectable in tissue from mice with targeted deletion of laminin-411 (confirming laminin-411 as a major tissue ligand); anti-MCAM antibody and soluble MCAM-Fc inhibited T cell adhesion to laminin-411 and reduced TH17 cell infiltration into the CNS in a mouse MS model. |
Solid-phase binding assay (MCAM-Fc to purified laminin), biolayer interferometry/affinity measurement (KD = 27 nM), laminin-411 knockout mouse tissue binding, in vitro T cell adhesion assay, in vivo EAE mouse model with antibody blockade |
PloS one |
High |
22792325
|
| 2014 |
Laminin-421, but not laminin-411, binds MCAM (CD146) in solid-phase binding assays; a function-blocking anti-MCAM antibody inhibits tumor cell migration on laminin-421 but not laminin-411, demonstrating that MCAM specifically mediates laminin-421-dependent tumor cell migration. |
Solid-phase binding assay (multiple laminin isoforms vs. MCAM), function-blocking antibody to MCAM, tumor cell migration assay on laminin substrates |
Matrix biology |
Medium |
24951930
|
| 2015 |
CD146 is identified as a receptor for netrin-1; netrin-1 binds CD146 with high affinity, inducing endothelial cell activation and downstream signaling in a CD146-dependent manner; conditional knockout of cd146 in murine endothelium or disruption of netrin-CD146 interaction by anti-CD146 antibody blocks netrin-1-induced angiogenesis; CD146 knockdown in zebrafish phenocopies netrin-1 loss-of-function vascular defects. |
Binding affinity assay, CD146 conditional knockout in mouse endothelium, anti-CD146 antibody blockade, zebrafish knockdown of CD146 and netrin-1a, ectopic netrin-1 overexpression with CD146 knockdown |
Cell research |
High |
25656845
|
| 2009 |
PAR1 mediates MCAM/MUC18 expression in metastatic melanoma via activation of PAFR and CREB phosphorylation; PAR1 silencing reduces PAFR expression and PAF production; PAFR silencing blocks MCAM expression; re-expression of PAFR in PAR1-silenced cells rescues MCAM expression; this PAR1-PAFR-MCAM pathway mediates melanoma adhesion to endothelial cells, transendothelial migration, and metastatic lung retention. |
shRNA silencing of PAR1 and PAFR, PAFR rescue in PAR1-silenced cells, CREB phosphorylation assay, ChIP for CREB binding to MCAM promoter, Western blot, transendothelial migration assay, in vivo metastasis model |
The Journal of biological chemistry |
High |
19703903
|
| 2011 |
MUC18/MCAM regulates Id-1 expression at the transcriptional level via ATF-3; MUC18 silencing upregulates ATF-3 which binds the Id-1 promoter (confirmed by ChIP) and represses Id-1; MUC18 rescue reverses Id-1 and ATF-3 expression patterns; Id-1 overexpression in MUC18-silenced cells restores MMP-2 expression and activity, linking the MUC18–ATF-3–Id-1 axis to melanoma invasion. |
Stable shRNA silencing of MUC18, cDNA microarray, ChIP for ATF-3 binding to Id-1 promoter, MUC18 rescue transfection, Id-1 overexpression rescue, MMP-2 activity assay (zymography) |
Cancer research |
High |
21467165
|
| 2012 |
MCAM silencing in ovarian cancer cells increases apoptosis and reduces cell spreading and invasion; these effects are associated with dysregulation of small RhoGTPases RhoA and Cdc42, placing MCAM upstream of Rho GTPase signaling. |
RNA interference (siRNA) knockdown of MCAM in SKOV-3 cells, apoptosis assay, invasion assay, RhoA/Cdc42 activity measurement |
Tumour biology |
Low |
22610942
|
| 2017 |
CD146 functions as a co-receptor of PDGF receptor-β to mediate pericyte recruitment to cerebrovascular endothelial cells during blood-brain barrier development; pericyte-specific Cd146 deletion impairs pericyte coverage and BBB integrity; the attached pericytes in turn downregulate endothelial CD146 by secreting TGF-β1, promoting further BBB maturation; endothelial-specific Cd146 deletion reduces claudin-5 expression and causes BBB breakdown. |
Endothelial-specific and pericyte-specific Cd146 conditional knockout mice, TGF-β1 treatment experiments, immunofluorescence, BBB integrity assay, claudin-5 expression analysis |
PNAS |
High |
28827364
|
| 2017 |
CD146 on macrophages drives foam cell formation by promoting internalization of scavenger receptor CD36 during lipid uptake; macrophage-specific Cd146 deletion reduces complex plaques in ApoE−/− mice on high-fat diet, with lipid-loaded macrophages exiting plaques; blocking CD146 restores migratory capacity of macrophages toward CCL19/CCL21 that is reduced by oxLDL. |
Macrophage-specific Cd146 conditional knockout in ApoE−/− mice, CD36 internalization assay, anti-CD146 antibody treatment, oxLDL stimulation assay, transwell migration assay, atherosclerosis plaque analysis |
Cell research |
High |
28084332
|
| 2017 |
MCAM mediates chemoresistance in small-cell lung cancer via the PI3K/AKT/SOX2 signaling pathway; MCAM depletion reduces SOX2-dependent upregulation of MRP1/ABCC1 and reduces PI3K/AKT activity, sensitizing cells to chemotherapy; MCAM also modulates lactate production in a metabolic reprogramming context. |
MCAM depletion (siRNA/shRNA) in chemoresistant SCLC cells and PDX models, IC50 chemotherapy assay, PI3K/AKT pathway analysis, SOX2/MRP1 expression analysis, metabolomic profiling |
Cancer research |
Medium |
28646020
|
| 2017 |
KDM3A positively regulates MCAM expression in Ewing Sarcoma through both a direct mechanism (modulation of H3K9 methylation at the MCAM promoter) and an indirect mechanism (via the Ets1 transcription factor); MCAM depletion inhibits cell migration and experimental metastasis and partially rescues impaired migration caused by KDM3A knockdown. |
Global gene expression profiling (microarray), KDM3A and MCAM siRNA/shRNA knockdown, MCAM rescue in KDM3A-depleted cells, H3K9 methylation analysis at MCAM promoter (ChIP), Ets1 mechanistic analysis, in vitro migration assay, in vivo experimental metastasis model |
Oncogene |
High |
28319067
|
| 2017 |
MCAM (CD146) is required for VEGF-C-induced lymphatic sprouting; CD146 selectively activates p38 kinase downstream of VEGF-C to regulate sprouting, and also activates ERK to mediate VEGF-C-regulated proliferation and migration of lymphatic endothelial cells; CD146 knockdown in zebrafish phenocopies VEGF-C loss-of-function defects in lymphangiogenesis. |
CD146 knockdown in lymphatic endothelial cells (in vitro sprouting assay), p38 and ERK inhibition/activation, zebrafish CD146 knockdown and VEGF-C manipulation, in vivo lymphangiogenesis assays |
Scientific reports |
Medium |
28785085
|
| 2017 |
MCAM is an independent receptor for FGF4 and a membrane anchor of PLC-γ, acting as an upstream receptor of NFAT and a constitutive activator of JNK; MCAM-mediated vesicular trafficking toward FGF4 and NFAT transcriptional response determines lumenogenesis, while MCAM-driven JNK activation (independently of FGF signals) is required for ciliogenesis; mcam-deficient zebrafish and Xenopus exhibit global left-right asymmetry defects. |
Receptor identification for FGF4 (binding assay), PLC-γ co-immunoprecipitation, NFAT reporter assay, JNK activation assay, mcam genetic loss-of-function in zebrafish and Xenopus, lumenogenesis and ciliogenesis assays |
Nature communications |
High |
28589943
|
| 2017 |
Galectin-3 binds to N-linked glycans on CD146, inducing CD146 dimerization and subsequent AKT signaling activation; siRNA-mediated suppression of CD146 completely abolishes galectin-3-induced secretion of IL-6 and G-CSF from endothelial cells; galectin-3 binding site on CD146 is in Domain 5, which contains poly-N-acetyllactosamine sites. |
Galectin-3 affinity purification, co-localization (confocal microscopy), pull-down assay, gel filtration, biolayer interferometry (KD ~1.1 μM), mass spectrometry for N-glycosites, PNGase F treatment, domain deletion mutants, siRNA knockdown, cytokine ELISA |
The Journal of biological chemistry |
High |
28364041
|
| 2018 |
CD146 mediates a cadherin switch during TGF-β-induced EMT: TGF-β induces CD146 expression; CD146 positively correlates with STAT3/Twist activation (which inhibits E-cadherin) and ERK pathway activation (which enhances N-cadherin); CD146-deficient MEFs exhibit decreased motility due to reversion of the cadherin switch. |
TGF-β-induced EMT model, CD146 overexpression and knockout (in MEFs), Western blot for STAT3/Twist/ERK/cadherins, cell motility assay, correlation with ovarian cancer patient outcome |
Cancer letters |
Medium |
29777784
|
| 2019 |
CD146 and HIF-1α engage in cross-regulation in pulmonary artery smooth muscle cells: CD146 expression reinforces HIF-1α transcriptional program and vice versa; smooth-muscle-specific Cd146 genetic ablation mitigates pulmonary vascular remodeling in chronic hypoxic mice; anti-CD146 antibodies alleviate established pulmonary hypertension and enhance cardiac function in two rodent models. |
Smooth-muscle-specific Cd146 conditional knockout, chronic hypoxia mouse model, two pharmacological rodent PH models with anti-CD146 antibody treatment, HIF-1α pathway analysis, hemodynamic measurements |
Nature communications |
High |
31391533
|
| 2019 |
S100A8/A9 binds to MCAM (CD146) on breast cancer cell surface and activates ETV4 downstream; ETV4 transcriptionally upregulates ZEB1 to induce EMT; downregulation of MCAM or ETV4 represses EMT and reduces tumor growth and lung metastasis in vivo. |
Co-immunoprecipitation/binding assay (S100A8/A9–MCAM interaction), MCAM and ETV4 knockdown, ZEB1 promoter analysis, EMT marker assessment, in vivo xenograft tumor and metastasis models |
Neoplasia |
Medium |
31100639
|
| 2019 |
ZBTB7A directly binds to the MCAM promoter and transcriptionally represses MCAM expression; ZBTB7A downregulation results in marked upregulation of MCAM and enhanced melanoma cell invasion and metastasis; an inverse correlation between ZBTB7A and MCAM expression is validated in human melanoma specimens. |
ChIP demonstrating ZBTB7A binding to MCAM promoter, ZBTB7A knockdown/overexpression, invasion and metastasis assays, human melanoma tissue gene expression analysis |
Molecular cancer research |
Medium |
25995384
|
| 2021 |
CD146 directly interacts with the SH3 domain of coreceptor-free LCK via its cytoplasmic domain in T cells; CD146 forms monomers and dimers, with dimerized CD146 increasing after TCR ligation; increased dimerized CD146 recruits LCK and promotes LCK autophosphorylation, thereby initiating TCR signaling; CD146 deficiency in T cells substantially impairs thymocyte development and peripheral activation; in tumor models, CD146 deficiency impairs antitumor T cell responses. |
Co-immunoprecipitation (CD146–LCK SH3 domain interaction), CD146 cytoplasmic domain deletion analysis, native PAGE and crosslinking for dimer analysis, T cell-specific Cd146 conditional knockout mice, thymocyte development assay, TCR signaling assays, tumor models |
The Journal of clinical investigation |
High |
34491908
|
| 2018 |
CD146 interacts with the CD146 ectodomain via galectin-3 binding; galectin-3 binds CD146 ectodomain with KD ~1.1 μM (biolayer interferometry); galectin-3 interaction requires N-glycans on CD146, with Domain 5 (containing poly-N-acetyllactosamine sites) as the binding site; CD146 knockdown significantly attenuates galectin-3-mediated endothelial cell migration. |
Galectin-3 pulldown assay, gel filtration, biolayer interferometry, N-glycan removal (PNGase F), domain deletion mutants, CD146 knockdown, endothelial cell migration assay |
FEBS letters |
Medium |
29741757
|
| 2021 |
HERV-K dUTPase interaction with MCAM is necessary to upregulate VCAM1 in pulmonary arterial endothelial cells; MCAM engagement by HERV-K dUTPase activates p-p38/NF-κB and pERK1/2-ATF2 signaling to increase VCAM1, contributing to endothelial mesenchymal transition. |
HERV-K dUTPase overexpression in monocytes, extracellular vesicle application to endothelial cells, MCAM blockade/knockdown, p38/NF-κB and ERK/ATF2 pathway analysis, VCAM1 measurement, EndMT marker analysis |
JCI insight |
Medium |
34185707
|
| 2023 |
Netrin-1 induces formation of a CD146-Gαi1/3-Gab1 complex: Gαi1/3 associate with CD146 upon Netrin-1 stimulation, facilitating CD146 internalization, Gab1 recruitment, and downstream Akt-mTOR and Erk activation; silencing or knockout of Gαi1/3 inhibits Netrin-1-induced endothelial cell proliferation, migration, and tube formation; endothelial Gαi1/3 knockdown in mice inhibits Netrin-1-induced retinal angiogenesis. |
Co-immunoprecipitation (Gαi1/3–CD146 interaction), Gαi1/3 siRNA/shRNA and knockout in MEFs and endothelial cells, Gαi1/3 dominant-negative mutants, Gab1 knockout, CD146 internalization assay, Akt/ERK phosphorylation, HUVEC functional assays (proliferation, migration, tube formation), in vivo retinal angiogenesis (AAV shRNA delivery in mice) |
Theranostics |
High |
37153740
|
| 2014 |
MUC18 overexpression in airway epithelial cells promotes IL-8 production while inhibiting IFN-β expression after polyI:C stimulation or HRV infection; increased serine phosphorylation of MUC18 correlates with its pro-inflammatory function; ERK inhibition reduces MUC18 serine phosphorylation and IL-8 production, placing MUC18 in an ERK-dependent pro-inflammatory signaling pathway. |
Lentiviral MUC18 overexpression in primary airway epithelial cells, polyI:C stimulation and HRV infection, cytokine ELISA (IL-8, IFN-β), serine phosphorylation analysis, ERK inhibitor treatment |
Journal of clinical & cellular immunology |
Medium |
25478290
|
| 2012 |
MUC18/CD146 amplifies proinflammatory responses in alveolar macrophages during bacterial infection; Muc18−/− mice show lower lung KC, TNF-α, and neutrophil recruitment after Mycoplasma pneumoniae infection; adenovirus-mediated MUC18 gene transfer into Muc18−/− alveolar macrophages restores KC production; MUC18 enhances NF-κB activation in macrophages. |
Muc18 knockout mice, intratracheal M. pneumoniae infection, cytokine/chemokine ELISA, adenoviral MUC18 gene transfer rescue, NF-κB activation assay |
The American journal of pathology |
High |
23256918
|
| 2022 |
ST6GAL1-mediated α2,6-sialylation of MCAM inhibits MCAM interaction with galectin-3 and decreases MCAM expression on the cell surface, thereby suppressing HCC cell migration and invasion; sialylated MCAM levels negatively correlate with tumor malignancy in HCC patients. |
Metabolic labeling-based glycoproteomics, ST6GAL1 overexpression, co-immunoprecipitation (MCAM–galectin-3 after sialylation manipulation), flow cytometry for surface MCAM, migration/invasion assays in vitro, in vivo xenograft metastasis model |
Oncogene |
Medium |
36528750
|
| 2022 |
CD146 forms a co-receptor complex with integrin β1 and activates YAP signaling by regulating LATS1 phosphorylation; this drives nuclear translocation of YAP, promotes DNA damage repair, EMT, and stemness, and confers radioresistance; dual inhibition of CD146 and integrin β1 synergistically increases breast cancer sensitivity to radiotherapy. |
Co-immunoprecipitation (CD146–integrin β1), CD146 knockdown/overexpression, LATS1/YAP phosphorylation and localization analysis, DNA damage repair assay, in vitro and in vivo radioresistance models, dual inhibition experiments |
Cancer letters |
Medium |
35944750
|
| 2023 |
CD146 acts as a protective shield against DCBLD2 protein degradation in breast phyllodes tumor cells; by preventing DCBLD2 degradation, CD146 activates the PI3K/AKT signaling pathway, enhancing malignant behaviors; this was demonstrated by co-immunoprecipitation and pull-down assays identifying the CD146–DCBLD2 interaction. |
Co-immunoprecipitation, pull-down assay (CD146–DCBLD2 interaction), transcriptome sequencing, proteomic analysis, DCBLD2 degradation assay, PI3K/AKT pathway analysis, organoid and PDX models with anti-CD146 antibody AA98 |
Cancer communications |
Medium |
37856423
|
| 2023 |
CD146 inhibits TMEM176B (an immunoregulatory cation channel) activity in tumor-associated macrophages to facilitate NLRP3 inflammasome activation; CD146 expression in macrophages is negatively controlled by STAT3 signaling; CD146+ TAMs exert antitumor activity, and reducing this population promotes myeloid-derived suppressor cell recruitment via JNK signaling. |
Flow cytometry and single-cell analysis of CD146+ TAM subpopulation, CD146 and STAT3 knockdown/manipulation, TMEM176B inhibitor treatment, NLRP3 inflammasome activation assay, JNK signaling analysis, in vivo tumor models |
Cellular & molecular immunology |
Medium |
37308559
|
| 2014 |
TNF-α upregulates endothelial CD146 expression through NF-κB transactivation; endothelial-specific Cd146 conditional knockout significantly ameliorates colitis severity and reduces tumor incidence in models of colitis-associated colorectal carcinogenesis; endothelial CD146 promotes both angiogenesis and proinflammatory leukocyte extravasation. |
Endothelial-specific Cd146 conditional knockout mice, TNF-α stimulation with NF-κB pathway analysis, two murine colitis models, colitis-associated carcinogenesis model, anti-CD146 antibody treatment |
The American journal of pathology |
High |
24767106
|
| 2018 |
CD146 blockade specifically impedes T cell migration across the choroid plexus (CP) into the CNS; MCAM-expressing T cells migrate through the CP where laminin-411 is expressed in endothelial basement membranes; anti-MCAM antibody reduces in vitro transmigration of MCAM-expressing T cells across laminin α4-expressing barriers and delayed disease onset in CD4::Itga4−/− mice when VLA-4 is absent. |
Anti-MCAM antibody treatment in murine EAE and CP-dependent CNS inflammation models, T cell-specific α4-integrin conditional KO, in vitro human T cell transmigration assay through fibroblast-derived ECM and brain endothelial monolayer, laminin α4 detection in mouse and human CP tissue |
Journal of neuroinflammation |
High |
30134924
|
| 1997 |
MUC18/MCAM (CD146) is neo-expressed on human T cells upon activation (reaching maximum at day 3 post-PHA stimulation); MUC18/MCAM is expressed on CD3+ T cells in delayed-type hypersensitivity lesions, synovial fluid T cells in rheumatoid arthritis, and T leukemia cells, suggesting a role in activated T cell extravasation and homing. |
mAb characterization (molecular weight, cDNA-transfected L cell reactivity, N-terminal sequencing, immunoblot), flow cytometry of activated peripheral blood T cells, immunohistochemistry of tissue specimens |
Journal of immunology |
Medium |
9036955
|
| 2014 |
Semaphorin 3A (Sema3A) upregulates MelCAM/MCAM expression through a NRP-1–PTEN–FOXO3a pathway; FOXO3a directly regulates MelCAM at the transcriptional level (demonstrated by ChIP and EMSA), and Sema3A-induced NRP-1-mediated PTEN-dependent FOXO3a activation results in MelCAM upregulation, suppressing breast cancer cell migration, tumor growth, and angiogenesis. |
Sema3A treatment, NRP-1/PTEN/FOXO3a knockdown/overexpression, ChIP for FOXO3a binding to MelCAM promoter, EMSA, nuclear translocation analysis, in vivo tumor and angiogenesis assays |
Oncogene |
Medium |
24727891
|
| 2020 |
SOX18 transcriptionally activates MCAM by directly binding to the MCAM promoter; MCAM knockdown decreases SOX18-mediated gastric cancer invasion and metastasis, while MCAM overexpression rescues the invasion/metastasis defect caused by SOX18 inhibition; CCL7-CCR1-ERK/ELK1-SOX18 forms a positive feedback loop that drives GC metastasis. |
ChIP for SOX18 binding to MCAM promoter, MCAM and CCL7 knockdown/overexpression in SOX18 manipulation context, in vitro invasion assay, in vivo metastasis models, ERK/ELK1 pathway analysis, CCR1 inhibitor treatment |
Oncogene |
Medium |
32616889
|