Recombinant Human CST2 /Cystatin-SA Protein
- Known as:
- Recombinant Human CST2 /Cystatin-SA Protein
- Catalog number:
- cs-056
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human CST2 /Cystatin- Protein
Related genes to: Recombinant Human CST2 /Cystatin-SA Protein
- Gene:
- CST2 NIH gene
- Name:
- cystatin SA
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1990-02-06
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human CST2 /Cystatin-SA Protein
Related articles to: Recombinant Human CST2 /Cystatin-SA Protein
- Smoking is a preventable cause of colorectal cancer (CRC), and nicotine metabolism may promote tumorigenesis. We aimed to investigate the prognostic significance of nicotine metabolism‑related genes (NRGs) in colon adenocarcinoma (COAD) and to develop a gene signature for patient stratification. - Source: PubMed
Publication date: 2026/02/11
Li JunliangZhang JunyiWang DanningShen JieyiShen ChongZeng WeiqiWang Jianwei - Hippo is the namesake component of a conserved transduction cascade/regulator of tissue homeostasis and development across metazoans. The Ste20 family kinase Hippo/MST activates the NDR family kinase Warts/LATS to inhibit the transcriptional coactivator Yorkie/YAP/TAZ and its transcription factor partner Scalloped/TEAD. In Caenorhabditis elegans, cell lineages and organ sizes are largely invariant, and classical Hippo phenotypes such as tissue overgrowth are absent. Nevertheless, WTS-1, YAP-1, and the TEAD-like transcription factor EGL-44 form a conserved core module required for larval development past the L2 stage. Crucially, a direct role for Hippo signaling remains unestablished. To address this question, we generated a fluorescently tagged endogenous YAP-1 as a live biomarker of pathway activity. Upon WTS-1 loss, endogenous YAP-1 translocated from cytosol to nucleus in epithelium and intestine. Tissue-specific depletion revealed that intestinal but not epithelial WTS-1 is essential for progression past L2. The duplicated Hippo-related kinases CST-1 and CST-2 repressed YAP-1 nuclear localization in the epithelium but not intestine, indicating that intestinal WTS-1 functions without CST-1/2. The Ste20 kinase MIG-15, orthologous to Drosophila Misshapen and mammalian MAP4K4/6/7, was redundant with CST-1/2 for larval progression. Yet deficient MIG-15 uniquely increased YAP-1 abundance without driving nuclear localization. By contrast, the Ste20 kinase GCK-2, orthologous to Drosophila Happyhour and mammalian MAP4K1/2/3/5, had no detectable role. Our findings establish C. elegans as a model for Hippo signaling, with Hippo-dependent and -independent cascades controlling WTS-1 in epithelia and intestine, respectively. In this context, YAP-1/EGL-44 outputs are repurposed from the conventional association with growth control to non-proliferative developmental functions. - Source: PubMed
Publication date: 2026/02/26
Huynh LinhFakieh Razan AHendrix C'BrionnePowell ReidReiner David J - Lung cancer patients with interstitial pneumonia (IP) have limited treatment options due to the risks associated with therapeutic intervention. The underlying causes of IP in these patients are diverse, and there is currently no detailed molecular pathological classification or an established understanding of the effectiveness of anti-fibrotic medications such as nintedanib. This study aimed to elucidate the mechanism of action of nintedanib by analyzing differential RNA expression between normal and fibrotic lung tissues from lung cancer patients with IP. - Source: PubMed
Publication date: 2026/02/05
Kuroda HiroakiMasago KatsuhiroSeto KatsutoshiHorio YoshitsuguSasaki EiichiFujita ShiroMatsushita Hirokazu - Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide. Accumulating evidence suggests that dysregulation of cystatin SA (CST2) plays a pivotal role in tumor progression. However, the underlying mechanisms and clinical significance of CST2 in NSCLC remain unexplored, highlighting the need for a comprehensive investigation to identify potential therapeutic targets. The study recruited 69 NSCLC patients and purchased NSCLC cell lines including A549, PC-9, and H1299 as well as human bronchial epithelial cells (16HBE) for the study. The mRNA levels of CST2 and transcription factor AP-2 alpha (TFAP2A) were quantified using quantitative reverse transcription polymerase chain reaction, while their protein expression was assessed by western blotting or immunohistochemistry assay. Cell proliferation, apoptosis, migration, and invasion were analyzed using the 5-Ethynyl-2'-deoxyuridine assay, flow cytometry, wound-healing assay, transwell migration and invasion assays, respectively. Reactive oxygen species (ROS) levels and Fe concentrations were measured by flow cytometry and colorimetric assay, respectively. The chromatin immunoprecipitation (ChIP)assay and dual-luciferase reporter assay were employed to elucidate the relationship between TFAP2A and CST2. A xenograft mouse model assay was conducted to evaluate the effects of TFAP2A and CST2 on the malignant progression of H1299 and A549 cells. The results showed that CST2 expression was found to be upregulated in NSCLC tissues and cells. CST2 promoted the proliferation, migration and invasion of H1299 and A549 cells, while inhibiting apoptosis, oxidative stress, and ferroptosis. TFAP2A transcriptionally activated CST2 in both H1299 and A549 cells, leading to the promotion in tumor progression in vitro. Similarly, TFAP2A enhanced the malignant progression of NSCLC cells in vivo by upregulating CST2 expression. Therefore, TFAP2A transcriptionally activated CST2, contributing to the malignant progression of NSCLC. These findings underscored the potential clinical significance of targeting the TFAP2A/CST2 axis as a novel therapeutic strategy for the treatment of NSCLC. - Source: PubMed
Li ChuankuiWang GuowenTao TaoYang YifanLi QicaiSang HaiweiWang Zuyi - Ovarian cancers with similar histopathologic but diverse immunogenomic profiles may require different treatment regimens to achieve the best clinical outcomes. The development of optimal treatment regimens will thus require an understanding of the main ways in which ovarian cancers differ with respect to their immunogenomic profiles. We used a multimodal latent variable model to enable an integrated analysis of somatic mutation, mRNA expression, and multiplex immunofluorescence data to uncover the principal drivers of intertumor heterogeneity across 197 patients with ovarian cancer. We found that the majority of the immunogenomic intertumor heterogeneity was driven by gene expression and immune infiltration in the tumor core and invasive margin. Moreover, much of this heterogeneity could not be explained by histologic subtype; somatic mutation patterns explained much of the difference between high-grade serous and other subtypes. Clustering of samples according to their positions in the latent space revealed a distinct subgroup of endometrioid ovarian cancer tumors, characterized by increased CST2 expression and improved prognosis, among other immunogenomic features. We identified a group of collagen-related genes, for which expression in all subtypes was inversely correlated with the density of proliferating tumor cells in the tumor core and associated with increased levels of inflammatory fibroblasts, independent of tumor purity. In summary, our findings advocate for a paradigm shift in how we classify and approach the treatment of ovarian cancer. By moving beyond the constraints of histologic subtypes and delving into the molecular intricacies of patient-specific tumor microenvironments, we unveil a new opportunity for targeted immuno-oncological treatment of a subset of patients with ovarian cancer. - Source: PubMed
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