Integrin alphavbeta6 mediates epithelial-mesenchymal transition in human bronchial epithelial cells induced by lipopolysaccharides of Pseudomonas aeruginosa via TGF-beta1-Smad2/3 signaling pathway.
These findings provide insights into the molecular mechanism underlying ITGB6 overexpression in oral squamous cell carcinomas and may have important implications for therapeutic purposes.
Results show that interleukin-6 (IL-6) and integrin alphavbeta6 (integrin alphanubeta6) are indicators of cancer progression and poor prognosis in patients with colon cancer.
ITGB6 is present in the serum of colorectal carcinoma (CRC) but not in non-CRC control patients predicted the onset of metastatic disease and was associated with poor prognosis.
Oncolytic Ad5NULL-A20 virotherapies represent an excellent vector for local and systemic targeting of alpha5 beta 6-overexpressing cancers and exciting platforms for tumor-selective overexpression of therapeutic anticancer modalities including immune checkpoint inhibitors.
differential expression of alphavbeta3 and alphavbeta6 was examined in MDA-MB-231 MDA-MB-468 and MCF-10A cells which signify three different stages of breast cancer development from highly metastatic to non-tumorigenic stage.
Integrin alpha5beta6 down-regulation causes a significant increase in donor cancer cells and their exosomes of two molecules that have a tumor suppressive role STAT1 and MX1.
these findings demonstrate that JunB and CBP-mediated histone hyperacetylation are responsible for TGF-beta1 induced ITGB6 transcription in oral squamous cell carcinoma (OSCC) cells suggesting that epigenetic mechanisms are responsible for the active transcription expression of ITGB6 induced by TGF-beta1 in OSCC cells.
Integrin alphanubeta6 can mediate the MAPK signal pathway of the cells and regulate the expression of CyclinB1 and the apoptosis-related proteins like Bcl-x1 and Caspase-2 thus affecting the process of the proliferation and apoptosis of thyroid carcinoma cells.
Eps8/Abi1/Sos1 tricomplex acts as a key molecular switch altering the balance between Rac1 and Rho activation; its presence or absence in pancreatic ductal adenocarcinoma cells modulates alphavbeta6-dependent functions resulting in a pro-migratory (Rac1-dependent) or a pro-TGF-beta1 activation (Rho-dependent) functional phenotype.
first PET/CT scans of head and neck squamous cell carcinoma (HNSCC) and NSCLC patients displayed SFITGv6 accumulation specifically in tumors but not in inflammatory lesions.Thus SFITGv6 represents a novel powerful tracer for imaging and possibly for endoradiotherapy of ITGa5b6-positive carcinoma
Treatment of these cells with the dual-specificity tyrosine-kinase inhibitor lapatinib led to downregulation of epithelial-to-mesenchymal transition as indicated by lower levels of SNAI1 and SNAI2 transcripts integrin AVB6 and matrix metalloproteinase 9 protein
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