Publications by authors named "S Nishimatsu"
Objective: We previously reported that dickkopf WNT signaling pathway inhibitor 3 (DKK3) expression is correlated with poorer prognosis in head and neck squamous cell carcinoma (HNSCC). Here we investigated DKK3 expression by using The Cancer Genome Atlas (TCGA) public database and bioinformatic analyses.
Methods: We used the RNA sequence data and divided the tumor samples into "DKK3-high" and "DKK3-low" groups according to median DKK3 expression.
Article Synopsis
- α-Klotho is a protein linked to longevity, and its deficiency in mice leads to reduced lifespan and significant muscle deterioration.
- Loss of circulating α-Klotho correlates with increased activation of Smad2, which is involved in aging-related muscle wasting caused by TGF-β factors.
- Treatment with a small-molecule inhibitor, Ki26894, shows promise in reversing muscle atrophy and enhancing muscle fiber type in aged mice, suggesting a potential therapeutic approach to combat age-related muscle loss.
Background: Head and neck squamous cell carcinoma (HNSCC) is the most common malignant tumor of the head and neck. We identified cancer-specific genes in HNSCC and focused on DKK3 expression. DKK3 gene codes two isoforms of proteins (secreted and non-secreted) with two distinct cysteine rich domains (CRDs).
View Article and Find Full Text PDFCaveolin 3 suppresses phosphorylation-dependent activation of sarcolemmal nNOS.
Biochem Biophys Res Commun
November 2022
Article Synopsis
- Mutations in the caveolin 3 gene are linked to autosomal dominant limb-girdle muscular dystrophy (LGMD)1C, causing loss of caveolin 3 and myofiber shrinkage in mice.
- Caveolin 3 binds to neuronal nitric oxide synthase (nNOS) and prevents its activation at a specific site, affecting muscle cell behavior and size.
- Enhancing nNOS activity, either through genetic manipulation or exercise, can promote muscle growth and counteract the effects of caveolin 3 mutations, indicating a potential compensatory mechanism for muscle size regulation.
Objective: We previously reported that dickkopf WNT signaling inhibitor 3 (DKK3) would modulate malignant potential of oral squamous cell carcinoma (OSCC) via activating Akt. Recently, cytoskeleton associated protein 4 (CKAP4) functions as receptor of DKK3, which activates Akt in esophageal squamous cell carcinoma, but its expression and function in OSCC were unclear.
Methods: We studied DKK3 and CKAP4 protein expression in OSCC tissue and investigated the correlation between protein expression and clinical data.