Last update 01 Nov 2024

CILP

Last update 01 Nov 2024

Basic Info

Synonyms

cartilage intermediate layer protein, Cartilage intermediate layer protein 1, Cartilage intermediate layer protein 1 C1

+ [5]

Introduction

Probably plays a role in cartilage scaffolding. May act by antagonizing TGF-beta1 (TGFB1) and IGF1 functions. Has the ability to suppress IGF1-induced proliferation and sulfated proteoglycan synthesis, and inhibits ligand-induced IGF1R autophosphorylation. May inhibit TGFB1-mediated induction of cartilage matrix genes via its interaction with TGFB1. Overexpression may lead to impair chondrocyte growth and matrix repair and indirectly promote inorganic pyrophosphate (PPi) supersaturation in aging and osteoarthritis cartilage.

Drugs associated with CILP

WO2024056833

Patent Mining

Target

CILP

Mechanism-

Active Org.

Nordic Bioscience A/S

Originator Org.

Nordic Bioscience A/S

Active Indication

Skin and Musculoskeletal Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CILP

100 Translational Medicine associated with CILP

0 Patents (Medical) associated with CILP

Literatures (Medical) associated with CILP

01 Dec 2024·Molecular Biology Reports

Cholesterol associated genetic risk score and acute coronary syndrome in Czech males

Article

Author: Kettner, Jiri ; Adamkova, Vera ; Mrázková, Jolana ; Lanska, Vera ; Pitha, Jan ; Kautzner, Josef ; Staněk, Vladimir ; Gebauerová, Marie ; Hubacek, Jaroslav A

AbstractBackgroundDespite a general decline in mean levels across populations, LDL-cholesterol levels remain a major risk factor for acute coronary syndrome (ACS). The APOB, LDL-R, CILP, and SORT-1 genes have been shown to contain variants that have significant effects on plasma cholesterol levels.Methods and resultsWe examined polymorphisms within these genes in 1191 controls and 929 patients with ACS. Only rs646776 within SORT-1 was significantly associated with a risk of ACS (P < 0.05, AA vs. + G comparison; OR 1.21; 95% CI 1.01–1.45). With regard to genetic risk score (GRS), the presence of at least 7 alleles associated with elevated cholesterol levels was connected with increased risk (P < 0.01) of ACS (OR 1.26; 95% CI 1.06–1.52). Neither total mortality nor CVD mortality in ACS subjects (follow up—9.84 ± 3.82 years) was associated with the SNPs analysed or cholesterol-associated GRS.ConclusionsWe conclude that, based on only a few potent SNPs known to affect plasma cholesterol, GRS has the potential to predict ACS risk, but not ACS associated mortality.

04 Oct 2024·Journal of Proteome Research

Proteomics Analysis of Renal Cell Line Caki-2 with AFMID Overexpression and Potential Biomarker Discovery in Urine

Article

Author: Sun, Wei ; Xu, Jiyu ; Sun, Jiameng ; Guo, Zhengguang ; Chang, Jinchun ; Sun, Haidan ; Liu, Xiaoyan

Aromatic caninurine formamase (AFMID) is an enzyme involved in the tryptophan pathway, metabolizing N-formylkynurenine to kynurenine. AFMID had been found significantly downregulated in clear cell renal cell carcinoma (ccRCC) in both tissue and urine samples. Although ccRCC is characterized by a typical Warburg-like phenotype, mitochondrial dysfunction, and elevated fat deposition, it is unknown whether AFMID plays a role in tumorigenesis and the development of ccRCC. In the present study, AFMID overexpression had inhibitory effects for ccRCC cells, decreasing the rate of cell proliferation. Quantitative proteomics showed that AFMID overexpression altered cellular signaling pathways involved in cell growth and cellular metabolism pathways, including lipid metabolism and inositol phosphate metabolism. Further urine proteomic analysis indicated that cellular function dysfunction with AFMID overexpression could be reflected in the urine. The activity of predicted upregulators DDX58, TREX1, TGFB1, SMARCA4, and TNF in ccRCC cells and urine showed opposing change trends. Potential urinary biomarkers were tentatively discovered and further validated using an independent cohort. The protein panel of APOC3, UMOD, and CILP achieved an AUC value of 0.862 for the training cohort and 0.883 for the validation cohort. The present study is of significance in terms of highlighting various aspects of pathway changes associated with AFMID enzymes, discovering potential specific biomarkers for potential patient diagnosis, and therapeutic targeting.

01 Jan 2024·Cancer Gene Therapy

CILP is a potential pan-cancer marker: combined silico study and in vitro analyses

Article

Author: Zhang, Sailong ; Guo, Bingjie ; Zhao, Feiran

CILP (Cartilage intermediate layer protein), an ECM (extracellular matrix) glycoprotein, is found to be associated with intervertebral disc degeneration, chronic heart failure, obese and cardiac fibrosis. However, there are few reports on the role of CILP in tumors. Thus, in this study, we mainly explored the function of CILP in the occurrence and development of tumors and whether it could be a potential pan-cancer marker. Pan-cancer data in this study were obtained from UCSC Xena. Single-cell data were obtained from GSE152938. ROC (Receiver operating characteristic) curves were used to evaluate the accuracy of CILP in predicting the occurrence of different tumor types. The Kaplan-Meier plots were used to assess the relationship between CILP expression and survival prognosis in different tumor types by COX regression analysis. Pseudotime analysis and cell communication analysis were used to further explore the function of CILP at Single cell level. The human RCC (renal cell carcinoma) cell lines ACHN and 786-O were used for further experimental verification. Bulk RNA-seq showed differences in CILP expression in several tumors. ROC curves showed that 14 tumors have AUC > 0.7. Kaplan-Meier plots indicated that CILP is a risk factor for patients in 3 kinds of tumors. ScRNA-seq (Single cell RNA sequencing) suggested that CILP might influence tumors through fibroblasts and cell-cell communication. Finally, we verified the function of CILP at the cellular level by using RCC cell lines ACHN and 786-O and found that knockdown of CILP could significantly inhibit migration and invasion. This finding supports that CILP could be a risk factor as well as a pan-cancer predictor for patients.

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CILP

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