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Last update 08 May 2025

CST6

Last update 08 May 2025

Basic Info

Synonyms

CST6, cystatin E/M, Cystatin-6

+ [2]

Introduction

High affinity inhibitor for cathepsin L, cathepsin L2 (cathepsin V), and legumain (PubMed:30425301). Involved in the regulation of epidermal cornification, and hair follicle morphogenesis and maintenance (PubMed:30425301).

Drugs associated with CST6

HG-1016

Target

CST6

Mechanism

CST6 modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Inflammation [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CST6

100 Translational Medicine associated with CST6

0 Patents (Medical) associated with CST6

160

Literatures (Medical) associated with CST6

01 Apr 2025·Molecular & Cellular Proteomics

Proteomic Analysis of Aqueous Humor Identified Clinically Relevant Molecular Targets for Neovascular Complications in Diabetic Retinopathy

Article

Author: Kim, Kwang Pyo ; Oh, Jae Won ; Jung, Jae Hun ; Kim, Tae Wan ; Ahn, Seong Joon

Diabetic retinopathy (DR) is a leading cause of blindness in adults under 40 in the developed world, with a significant proportion progressing to vision-threatening stages such as proliferative diabetic retinopathy (PDR) and neovascular glaucoma (NVG). This study aims to explore the molecular mechanisms underlying the progression from nonproliferative DR to PDR and NVG, focusing on identifying potential biomarkers and therapeutic targets. Utilizing discovery-based proteomics, specifically label-free quantification and tandem mass tag, we analyzed aqueous humor (AH) proteins obtained during cataract surgery or anterior chamber paracentesis from patients with nonproliferative DR, PDR, and NVG. Validation of marker candidates for each disease state was conducted using triple quadrupole-MS for targeted protein quantification. Our proteomic analysis identified 2255 proteins, and gene ontology analysis and functional annotation highlighted key biological processes implicated in DR, such as lens development, immune responses, and lipid metabolism. Validation of potential biomarkers identified 20 proteins with significant concentration changes, including several candidates with diagnostic utility based on ROC curve analysis. Further investigation into clinical relevance revealed that crystallin gamma-S is strongly associated with cataract severity, highlighting its role as a potential marker for ocular complications in DR. Importantly, we identified that the pathological factors driving DR progression have a much greater impact than age, a previously known variable, in shaping the proteomic landscape of AH. Additionally, proteins associated with macular degeneration (CA1, CA2, and HBA1) were uncovered, providing new insights into overlapping mechanisms between DR and other retinal diseases. Finally, proteins linked to panretinal photocoagulation treatment, including APOB and CST6, were identified, suggesting their involvement in the therapeutic response and post-treatment adaptation. These findings underscore the potential of AH proteomics in uncovering predictive biomarkers and elucidating the molecular pathogenesis of DR and its complications.

27 Feb 2025·Biochemical Society Transactions

Exploring the oncogenic roles of T-box transcription factor TBX2 and its potential as a therapeutic target

Review

Author: Mlaza, Mihlali V. ; Abrahams, Amaal ; Ali, Abid ; Bellis, Claire ; Prince, Sharon

During embryonic development, the T-box transcription factor TBX2 regulates key processes such as cell fate decisions, migration and tissue morphogenesis, and mutations that lead to reduced TBX2 levels result in developmental abnormalities including congenital heart and skeletal defects. TBX2, on the other hand, is overexpressed in a plethora of cancers where it functions as a powerful oncogene contributing to processes ranging from the bypass of senescence and cell death pathways to the promotion of cell proliferation, and epithelial-to-mesenchymal transition to drive invasion and metastasis. Additionally, TBX2 has been implicated in conferring resistance to anti-cancer drugs resulting in poor therapeutic outcomes. To exert its oncogenic functions, TBX2 transcriptionally represses key tumour suppressor genes involved in controlling cell proliferation and epithelial-to-mesenchymal transition such as p21Cip1, p14/p19ARF PTEN, NDRG1, CST6 and E-cadherin. This repression has been shown to involve complex mechanisms by which TBX2 co-opts transcription factors and recruits co-repression complexes to the promoters of these tumour suppressor genes. While limited information is available on how TBX2 is regulated in cancers, there is evidence that the levels and oncogenic functions of TBX2 are induced by developmental signalling pathways that are hijacked by cancer cells such as the Wnt/β-catenin and PI3K/AKT pathways. Understanding the complex molecular networks that TBX2 is involved in to exert its oncogenic functions is important because it may reveal potential therapeutic strategies for targeting TBX2 in TBX2-dependent cancers. This minireview discusses TBX2’s involvement in cancer signalling, its regulatory partners, and its impact on cancer progression and resistance to therapy.

13 Feb 2025·Antimicrobial Agents and Chemotherapy

Genetic interaction analysis of Candida glabrata transcription factors CST6 and UPC2A in the regulation of respiration and fluconazole susceptibility

Article

Author: Ollinger, Tomye L. ; Andes, David R. ; Kelly, Steven L. ; Stamnes, Mark A. ; Zarnowski, Robert ; Krysan, Damian J. ; Parker, Josie E.

ABSTRACTCandida glabrata is the second most common cause of invasive candidiasis and is widely known to have reduced susceptibility to fluconazole relative to many other Candida spp. Upc2A is a transcription factor that regulates ergosterol biosynthesis gene expression under conditions of sterol stress such as azole drug treatment or hypoxia. Through an in vitro microevolution experiment, we found that loss-of-function mutants of the ATF/CREB transcription factor CST6 suppresses the fluconazole hyper-susceptibility of the upc2A ∆ mutant. Here, we confirm that the cst6 ∆ upc2A ∆ mutants are resistant to fluconazole but not to hypoxia relative to the upc2A ∆ mutant. Sterol analysis of these mutants indicates that this suppression phenotype is not due to restoration of ergosterol levels in the cst6 ∆ upc2A ∆ mutant. Furthermore, increased expression of CDR1 , the efflux pump implicated in the vast majority of azole-resistant C. glabrata strains, does not account for the suppression phenotype. Instead, our data suggest that this effect is due in part to increased expression of the adhesin EPA3 , which has been shown by others to reduce fluconazole susceptibility in C. glabrata . In addition, we find that loss of both UPC2A and CST6 reduces the expression of mitochondrial and respiratory genes and that this also contributes to the suppression phenotype as well as to the resistance of cst6 ∆ to fluconazole. These latter data further emphasize the connection between mitochondrial function and azole susceptibility.

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CST6

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