^
Contact us  to learn more about
our Premium Content:  News alerts, weekly reports and conference planners
BIOMARKER:

CTSS overexpression

i
Other names: CTSS, Cathepsin S
Entrez ID:
Related biomarkers:
3ms
Prognostic value and immunological role of cathepsin S gene in pan‑cancer. (PubMed, Oncol Lett)
Functional enrichment analysis suggested that CTSS could drive a dynamic adjustment of biological functions and pathways in BLCA, SKCM, LGG and UVM, including immune response regulating signaling pathways, regulation of lymphocyte activation and T cell receptor singling pathways. The current study suggested that CTSS could be an essential biomarker for prognosis and immune infiltration features in multiple cancers.
Journal • Tumor mutational burden • PD(L)-1 Biomarker • IO biomarker • Pan tumor
|
TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • CD8 (cluster of differentiation 8) • PD-1 (Programmed cell death 1) • LAG3 (Lymphocyte Activating 3) • TIGIT (T Cell Immunoreceptor With Ig And ITIM Domains 2) • CD4 (CD4 Molecule) • CTSS (Cathepsin S)
|
LAG3 expression • CTSS overexpression
7ms
Cathepsin S activity controls chronic stress-induced muscle atrophy and dysfunction in mice. (PubMed, Cell Mol Life Sci)
In CC cells, CTSS silencing prevented stressed serum- and oxidative stress-induced IRS-2 protein reduction, loss of the myotube myosin heavy chain content, and apoptosis accompanied by a rectification of investigated molecular harmful changes; these changes were accelerated by CTSS overexpression. These findings demonstrated that CTSS plays a role in IRS-2-related protein anabolism and catabolism and cell apoptosis in stress-induced muscle wasting, suggesting a novel therapeutic strategy for the control of chronic stress-related muscle disease in mice under our experimental conditions by regulating CTSS activity.
Preclinical • Journal
|
BCL2 (B-cell CLL/lymphoma 2) • mTOR (Mechanistic target of rapamycin kinase) • IRS2 (Insulin receptor substrate 2) • CASP3 (Caspase 3) • CTSS (Cathepsin S)
|
CTSS overexpression
over1year
Polyglutamate-based nanoconjugates for image-guided surgery and post-operative melanoma metastases prevention. (PubMed, Theranostics)
To that end, a targeted treatment containing a BRAF (Dabrafenib - mDBF)/MEK (Selumetinib - SLM) inhibitors combined on one polymeric platform (PGA-SLM-mDBF) was evaluated for its anti-metastatic, preventive activity in combination with immune checkpoint inhibitors (ICPi) αPD1 and αCTLA4. Adjuvant therapy with PGA-SLM-mDBF combined with ICPi, was well-tolerated and resulted in prolonged survival and prevention of peritoneal and brain metastases formation in BRAF-mutated melanoma-bearing mice. The results reveal the great clinical potential of our PGA-based nanosystems as a tool for holistic melanoma treatment management.
Journal • PD(L)-1 Biomarker • IO biomarker
|
BRAF (B-raf proto-oncogene) • CTSS (Cathepsin S)
|
BRAF mutation • CTSS overexpression
|
Tafinlar (dabrafenib) • Koselugo (selumetinib)
over1year
Exploring the therapeutic vulnerabilities of cathepsin S hyperactive tumors (ITOC 2022)
In addition, CTSS hyperactive glioblastoma cell lines U-87 and U-251 also showed MCL-1 dependency following LMP, indicating that cytosolic CTSS hyperactivity primes for MCL-1 dependency across many cancer types. Conclusions Releasing CTSS from the lysosome is novel, attractive concept that can be combined with conventional, apoptosis-inducing therapies.
PARP Biomarker • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • MCL1 (Myeloid cell leukemia 1) • CTSS (Cathepsin S)
|
CTSS Y132D • CTSS overexpression
3years
Inhibition of Cathepsin S Restores TGF-β-induced Epithelial-to-mesenchymal Transition and Tight Junction Turnover in Glioblastoma Cells. (PubMed, J Cancer)
Our results proved that PI3K/AKT/mTOR pathway was significantly suppressed in the TGF-β+ZFL (CTSS inhibitor) groups, and AKT activator-SC79, could reverse the anti-invasion effect of CTSS, indicating an important role of PI3K/AKT/mTOR pathway in this process. Z-FL-COCHO (ZFL), a CTSS inhibitor, could reverse TGF-β-induced EMT and change of tight junction proteins via PI3K/AKT/mTOR pathway.
Journal
|
VIM (Vimentin) • TGFB1 (Transforming Growth Factor Beta 1) • CTSS (Cathepsin S)
|
CTSS overexpression
3years
Inhibition of JNK increases the sensitivity of hepatocellular carcinoma cells to lysosomotropic drugs via LAMP2A destabilization. (PubMed, Cell Death Discov)
The effect is cancer-specific, as JNK inhibition does not decrease LAMP2A in non-tumoral liver cells and does not alter their sensitivity to lysosomotropic drugs. Our finding on the new role of JNK as cancer-specific keeper of lysosomal homeostasis lays the ground for future evaluation of the efficacy of the combination of JNK inhibition and lysosomotropic agents as a potential therapeutic strategy in hepatocellular carcinoma.
Journal
|
CTSS (Cathepsin S)
|
CTSS overexpression