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Last update 08 May 2025

CST1

Last update 08 May 2025

Basic Info

Synonyms

CST1, Cystain-SA-I, cystatin SN

+ [3]

Introduction

Human saliva appears to contain several cysteine proteinase inhibitors that are immunologically related to cystatin S but that differ in their specificity due to amino acid sequence differences. Cystatin SN, with a pI of 7.5, is a much better inhibitor of papain and dipeptidyl peptidase I than is cystatin S, although both inhibit ficin equally well.

Drugs associated with CST1

Human endoderm stem cell (Chinese Academy of Sciences)

Target

CST1

Mechanism

CST1 modulators

Active Org.

Chinese Academy of Sciences

Originator Org.

Chinese Academy of Sciences

Active Indication

Liver Failure, Acute

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CST1

100 Translational Medicine associated with CST1

0 Patents (Medical) associated with CST1

237

Literatures (Medical) associated with CST1

01 Jun 2025·International Journal of Cancer

Induction of SOX17 with stimulation of WNT, TGF‐beta, and FGF signaling drives embryonal carcinomas into the yolk‐sac tumor lineage resulting in increased cisplatin resistance

Article

Author: Stephan, Alexa ; Raba, Katharina ; Fichtner, Alexander ; Kretschmer, Pia ; Skowron, Margaretha A. ; Köhrer, Karl ; Fuß, Janina ; Lautwein, Tobias ; Kotthoff, Mara ; Parmaksiz, Fatma ; Nettersheim, Daniel ; Bremmer, Felix

AbstractRelapsing germ cell tumor (GCT) patients often harbor components of the aggressive subtype yolk‐sac tumor (YST), suggesting that YST formation is an escape mechanism under therapy. Nevertheless, the molecular mechanisms inducing YST development from its stem cell‐like precursor embryonal carcinoma (EC) are largely unexplored. We demonstrated that the induction of the transcription factor SOX17 together with the stimulation of WNT, TGF‐beta / Activin, and FGF signaling drives EC cells into the YST lineage. Single cell RNA sequencing revealed that this cell fate switch was accompanied by the upregulation of the typical YST factors AFP, ANKRD1, APOA1, CST1, FOXA2, GATA6, and GPC3 and microRNAs, while pluripotency‐related genes NANOG, POU5F1, and SOX2 were downregulated. Chromatin immunoprecipitation followed by sequencing analysis revealed that SOX17 may act in concert with FOXA2 and GATA factors to initiate YST formation. Xenografting of the YST‐like cells into nude mice led to the growth of mixed GCT with YST components, confirming that these cells are able to form a YST in vivo. Moreover, the expression of cisplatin resistance factors was induced in a subpopulation of YST‐like cells, suggesting that the formation of a YST is accompanied by the acquisition of cisplatin resistance. Indeed, the YST‐like cells presented as less sensitive to cisplatin than their parental cells. Our study deciphered the molecular mechanisms forcing EC to differentiate into the YST lineage, which is accompanied by the acquisition of cisplatin resistance, confirming that YST formation is an escape mechanism for GCT under therapy. Thus, GCT patients should be screened for YST elements under therapy to identify patients at risk of developing therapy resistance.

01 Apr 2025·Archives of Biochemistry and Biophysics

Platelet-rich plasma Inhibits Ferroptosis and Inflammation to Alleviate Frozen Shoulder via Activating the CST1/GPX4 Signaling Pathway

Article

Author: Cai, Guangqing ; Ao, Zhijiang ; Ren, Zihao ; Li, Xing ; Wei, Licheng ; Hu, Zhen ; Xiang, Shengwen ; Hu, Weiguo ; Zhou, Yun

Platelet-rich plasma (PRP) has been shown to be beneficial to Frozen shoulder (FS), but the mechanism of PRP's intervention in FS is still incomplete. Ferroptosis and inflammation are important pathological factors of cartilage injury, but their role in FS has not been explored. In vivo, we found that PRP treatment significantly enhanced the joint range of motion and mitigated joint histopathological damage in FS rats. Notably, levels of iron ions, the ferroptosis marker prostaglandin-endoperoxide synthase 2 (PTGS2), reactive oxygen species (ROS), malondialdehyde (MDA), and pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) in the cartilage tissue of PRP-treated rats were significantly reduced. Conversely, levels of superoxide dismutase (SOD) and glutathione (GSH) were markedly increased. In vitro experiments revealed that PRP effectively countered the IL-1β-induced suppression of chondrocyte proliferation while also reducing levels of ferroptosis and inflammation. Furthermore, the CST1/GPX4 pathway was suppressed in the FS environment, while it has the potential to be activated by PRP. Importantly, silencing CST1 negated the therapeutic effects of PRP on IL-1β-treated chondrocytes and FS rats. In summary, we found that PRP alleviated the progression of FS by inhibiting ferroptosis and the inflammatory response by activating the CST1/GPX4 signaling pathway.

01 Mar 2025·European Journal of Clinical Microbiology & Infectious Diseases

Investigation of antimicrobial susceptibility and resistance gene prevalence in Capnocytophaga spp. isolated from dogs and cats and characterization of novel class A β-lactamase CST-1

Article

Author: Imaoka, Koichi ; Suzuki, Michio ; Umeda, Kaoru

PURPOSECapnocytophaga spp., common inhabitants of the animal oral cavity, are zoonotic pathogens transmitted to humans through dog/cat bites and cat scratches. Appropriate antimicrobial therapy is essential for treatment this zoonotic disease because of the rapid deterioration of systemic symptoms at disease onset; however, antimicrobial resistance of animal bite-associated Capnocytophaga spp. has not been fully investigated. We sought to understand the antimicrobial susceptibility and prevalence of resistance genes among Capnocytophaga sp. isolates obtained from dogs and cats.METHODMinimum inhibitory concentrations (MICs) of nine antibiotics for a total of 57 isolates belonging to 6 species (C. canimorsus, C. cynodegmi, C. canis, C. felis, C. stomatis, and C. catalasegens) were assayed using E-test. Resistance genes were detected using polymerase chain reaction, nucleotide sequencing, and whole-genome sequencing.RESULTSThe MICs of penicillin, ceftriaxone, cefepime, clindamycin, minocycline, nalidixic acid, and ciprofloxacin were high for some isolates. The MICs of imipenem and amoxicillin/clavulanic acid were low for all isolates. Known resistance genes bla_cfxA2, bla_OXA-347, emrF, and tetQ were detected using polymerase chain reaction. Mutation in the quinolone resistance-determining region of gyrA was also detected. Cst-1, a previously unreported gene, was identified using whole-genome analysis of two C. stomatis isolates. CST-1 was proposed as a class A, subclass A2, β-lactamase based on amino acid sequence and phylogenetic relationship. In recombination experiments, CST-1 inactivated penicillin and first- and second-generation cephems; however, sulbactam inhibited it.CONCLUSIONKnown and novel resistance genes are prevalent among Capnocytophaga spp. in animal oral cavities. The findings have clinical implications, especially in antimicrobial treatment.

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CST1

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