| 2017 |
ITGB8 activates VAV-RAC1 signaling via FAK in endometrial epithelial cells: ITGB8 knockdown reduced phosphorylated-FAK, phosphorylated-VAV, and GTP-bound RAC1, and FAK inhibition also blocked VAV/RAC1 activation, establishing a functional ITGB8→FAK→VAV→RAC1 signaling axis required for blastocyst attachment. |
siRNA knockdown of ITGB8 in endometrial epithelial cells and uterus, FAK inhibition, measurement of phospho-FAK (Y397), phospho-VAV, RAC1-GTP pull-down, JAr spheroid attachment assay |
Scientific reports |
Medium |
28507287
|
| 2015 |
ITGB8 regulates activation of latent TGF-β1 in the uterus: bioneutralization or mRNA silencing of Itgb8 at the preimplantation stage reduced active TGF-β1 release and downstream SMAD2/3 phosphorylation, linking ITGB8 to TGF-β1 activation during embryo implantation. |
Antibody-mediated bioneutralization of ITGB8, siRNA silencing in mouse uterus, measurement of active TGF-β1 and phospho-SMAD2/3, embryo implantation rate assessment |
Biology of reproduction |
Medium |
25788663
|
| 2015 |
ITGB8 overexpression is associated with gefitinib resistance in hepatic cancer cells, and ITGB8 silencing reverses resistance by reducing ABCB1, ABCC2, ABCG2, survivin, Bcl-2, and CDK1; the TGF-β pathway was implicated as a critical mediator of ITGB8-dependent drug resistance. |
siRNA knockdown of ITGB8 in HepG2/G cells, cell proliferation and apoptosis assays, Western blot for multidrug-resistance proteins and TGF-β pathway components |
International journal of clinical and experimental medicine |
Low |
25932283
|
| 2018 |
miR-199a-3p directly targets the 3'-UTR of ITGB8 and suppresses its expression; overexpression of ITGB8 rescued cisplatin resistance that was inhibited by miR-199a-3p, placing ITGB8 downstream of miR-199a-3p in control of cisplatin sensitivity in ovarian cancer cells. |
Luciferase reporter assay (3'-UTR binding), Western blot, miR-199a-3p overexpression/inhibition, ITGB8 rescue overexpression, cell proliferation, invasion, apoptosis, and in vivo orthotopic mouse model |
Oncology reports |
Medium |
29436681
|
| 2020 |
ITGB8 acts downstream of the lncRNA PVT1/miR-145-5p axis to activate the MEK/ERK signaling pathway in NSCLC; PVT1 knockdown suppressed ITGB8 expression and reduced MEK/ERK phosphorylation, while ITGB8 overexpression rescued these effects. |
siRNA/shRNA knockdown of PVT1, luciferase reporter assay for miR-145-5p binding, Western blot for p-MEK and p-ERK, ITGB8 rescue overexpression, xenograft tumor model |
Neoplasma |
Low |
32202906
|
| 2021 |
In goat endometrial epithelial cells, ITGB8 is a direct target of miR-187 (validated by 3'-UTR luciferase assay); inhibition of miR-187 upregulated ITGB8 and reduced FAK activity and cell proliferation, and both ITGB8 and miR-187 are regulated by interferon tau (IFNT), placing ITGB8 downstream of IFNT signaling during conceptus attachment. |
qRT-PCR, Western blot, dual-luciferase reporter assay in primary goat endometrial epithelial cells (EECs), miR-187 inhibition, FAK activity measurement |
Theriogenology |
Low |
34973644
|
| 2023 |
In bladder cancer, biomechanical stimuli from 3D Matrigel activate an F-actin/ITGB8/TRIM59/AKT/mTOR/glycolysis pathway; Western blotting confirmed upregulation of ITGB8, TRIM59, and phospho-AKT in soft tumor cells, and this axis was associated with tumor softness, stemness, and recurrence. |
Atomic force microscopy, microfluidic isolation of soft cells, Western blot for ITGB8/TRIM59/p-AKT/mTOR, double immunostaining for F-actin/TRIM59, colony formation assay, xenograft tumor model |
Chinese medical journal |
Low |
37390491
|
| 2026 |
Osteoblast-derived osteomodulin (OMD) engages integrin β8 on osteoclast precursors to suppress RhoA activity and enhance YAP phosphorylation, thereby reducing YAP/TEAD occupancy at the RRM2 promoter, repressing RRM2 transcription, decreasing mtDNA copy number and electron transport chain protein abundance, and reducing mitochondrial respiration and ATP production to restrain osteoclastogenesis. |
Osteoblast/MSC-specific and global Omd deletion mouse models, osteoclast precursor-specific deletion, recombinant OMD supplementation, pharmacologic RRM2 inhibition, ChIP (YAP/TEAD at RRM2 promoter), mitochondrial respiration assays, ITGB8-OMD interaction studies, ovariectomy and LPS bone-loss models |
Experimental & molecular medicine |
High |
41813908
|
| 2026 |
Transcription factor EBF1 directly regulates ITGB8 expression in bone marrow mesenchymal stromal cells (MSCs); MSC-specific deletion of Itgb8 or ITGB8-neutralizing antibody treatment in myelofibrosis mice reduced BM fibrosis, decreased MPL-mutant cell frequencies, and reduced BM inflammation, establishing ITGB8 as a downstream effector of EBF1 in the fibrotic MSC gene program. |
MSC-specific conditional Itgb8 knockout mice (MPL W515L transplant MF model), ITGB8-neutralizing antibody treatment, EBF1 ChIP/gene regulation studies, histology and flow cytometry for fibrosis and myeloid expansion |
bioRxivpreprint |
Medium |
41756923
|
| 2026 |
miR-199a-3p directly targets ITGB8 (confirmed by dual-luciferase reporter assay) and suppresses FAK-ERK-RUNX2 signaling in bone marrow mesenchymal stem cells; silencing miR-199a-3p restored ITGB8 levels and reactivated FAK-ERK-RUNX2, correcting the osteogenic/adipogenic differentiation imbalance in steroid-induced osteonecrosis of the femoral head. |
Dual-luciferase reporter assay, mRNA-seq, miR-199a-3p overexpression/inhibition in BMSCs, Western blot for phospho-FAK, phospho-ERK, RUNX2, antagomiR-199a-3p in vivo in SONFH rat model |
Research (Washington, D.C.) |
Medium |
41878635
|