CASP family x XIAP

Last update 08 May 2025

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CASP familyXIAP

100 Clinical Results associated with CASP family x XIAP

100 Translational Medicine associated with CASP family x XIAP

0 Patents (Medical) associated with CASP family x XIAP

1,660

Literatures (Medical) associated with CASP family x XIAP

01 May 2025·Biomaterials Advances

Etoposide-loaded lipopolymer nanoparticles promote Smac minetic activity against inhibitor of apoptosis protein for glioblastoma treatment

Article

Author: Kuo, Yung-Chih ; Lin, Chia-Wei ; Tai, Chien-Kuo

Encapsulated BV6 and SM164, two bivalent second mitochondria-derived activator of caspase (Smac) mimetics, in etoposide (ETO)-lipopolymer nanoparticles (NPs) have been developed to deplete inhibitor of apoptosis proteins (IAP), impair DNA, and produce antagonistic effects on glioblastoma multiforme (GBM) in nude mice. The NPs, composed of cocoa butter (CB) and polyvinyl alcohol (PVA), were stabilized by glycerol monostearate and Pluronic F-127, and grafted with transferrin (Tf) and wheat germ agglutinin (WGA) to dock the blood-brain barrier (BBB) and degenerated dopaminergic neurons. The dual-targeting NPs increased the BBB permeability of BV6, SM164 and ETO via recognizing Tf receptor (TfR) and N-acetylglucosamine that are abundantly expressed on brain microvascular endothelial cells. The sustained release of BV6, SM164 and ETO from CB-PVA-NPs for 48 h resulted in a reduction of about 40 % in the viability of U87MG cells and human brain cancer stem cells. Hematoxylin and eosin staining of the brain in GBM mice revealed atypical mitosis of cancer cells and a considerable decrease in tumor cell density after treatment with Tf-WGA-BV6-SM164-ETO-NPs. Compared to untreated mice, the current ETO preparation carrying Smac mimetics reduced cellular IAP-1 expression to about 33 % and X-linked IAP expression to about 42 %, while enhanced about 3.8-fold caspase-3, indicating the effectiveness of the nanocarriers in accelerating apoptosis of GBM cells. Tf-WGA-CB-PVA-NPs can be promising to upgrade BV6 and SM164 activity by ETO in clinical trials for GBM management.

01 May 2025·Developmental & Comparative Immunology

The class A scavenger receptor member 3 (SCARA3) regulates cell apoptosis through X-linked apoptosis inhibitory protein (XIAP) in turbot (Scophthalmus maximus L.)

Article

Author: Li, Chao ; Yang, Ning ; Zhuang, Xinghua ; Wang, Zhongyi ; Wang, Beibei ; Cao, Lili ; Li, Suwan ; Li, Honghong ; Chen, Xuan

Class A scavenger receptor 3 (SCARA3), a macrophage scavenger receptor-like protein, plays important roles in inhibiting cell proliferation, migration, and invasion. In the present study, a SCARA3 gene of turbot (SmSCARA3) (Gene ID: 118289953) with an 1815 bp ORF encoding 604 amino acids was identified. Phylogenetic analysis revealed that SmSCARA3 showed the closest relationship to that counterpart of olive flounder (Paralichthys olivaceus). The synteny analysis demonstrated conserved syntenic patterns across selected vertebrates. In addition, SmSCARA3 was ubiquitously expressed in all the examined tissues, with the highest expression level in intestine and the lowest expression level in the brain. SmSCARA3 exhibited different expression patterns in mucosal tissues (intestine, gill, skin) after two bacterial infections. Subsequently, recombinant SmSCARA3 protein (rSmSCARA3) revealed the strong binding affinity to LPS and responded primarily to LPS stimulation in intestinal cells of turbot. Additionally, the interference and overexpression experiments indicated that SmSCARA3 was associated with apoptosis related genes, such as Caspase1, Caspase3 and Caspase3a, and it could activate Caspase3 in HEPG2 cells. Moreover, flow cytometry revealed the apoptosis of SmSCARA3 overexpression group increased by 10.03%, which was consistent with the effect of SmSCARA3 on proliferation inhibition in intestinal cells of turbot. The cell apoptosis levels in the SmSCARA3-Flag and XIAP-HA experimental group were significantly lower than that in the control group (51.17% vs 72.72%). Finally, the Co-IP assay showed that SmSCARA3 could directly interact with XIAP. In conclusion, our results indicated that SmSCARA3 could activate Caspase3 and modulate apoptosis through XIAP , highlighting its potential roles as a therapeutic target for fish diseases.

01 Apr 2025·Animal Models and Experimental Medicine

The miR‐6779/XIAP axis alleviates IL‐1β‐induced chondrocyte senescence and extracellular matrix loss in osteoarthritis

Article

Author: Su, Jingyue ; Fang, Xiaoxiang ; Gao, Peng ; Chen, Xin ; Tang, Kexing ; Li, Zongchao ; Chen, Kun ; Deng, Zhenhan ; Yang, Shengwu ; Dai, Aonan ; Li, Liangjun

AbstractBackgroundOsteoarthritis (OA) is a long‐term degenerative joint disease worsening over time. Aging and chondrocyte senescence contribute to OA progression. MicroRNAs have been confirmed to regulate different cellular processes. They contribute to OA pathology and may help to identify novel biomarkers and therapies for OA.MethodsThis study used bioinformatics and experimental investigations to analyze and validate differentially expressed miRNAs in OA that might affect chondrocyte apoptosis and senescence.ResultsmiR‐6779 was found to be significantly down‐regulated in OA. Seventy‐six of the predicted and miR‐6779 targeted genes and the OA‐associated disease genes overlapped, and these were enriched in cell proliferation, cell apoptosis, and cell cycle. miR‐6779 overexpression remarkably attenuated IL‐1β effects on chondrocytes by reducing MMP3 and MMP13 levels, promoting cell apoptosis, suppressing cell senescence, and increasing caspase‐3, caspase‐9 and reducing P16 and P21 levels. miR‐6779 targeted inhibition of X‐linked inhibitor of apoptosis protein (XIAP) expression. XIAP knockdown partially improved IL‐1β‐induced chondrocyte senescence and dysfunction. Lastly, when co‐transfected with a miR‐6779 agomir, the XIAP overexpression vector partially attenuated the effects of miR‐6779 overexpression on chondrocytes; miR‐6779 improved IL‐1β‐induced senescence and dysfunction in chondrocytes through targeting XIAP.ConclusionmiR‐6779 is down‐regulated, and XIAP is up‐regulated in OA cartilage and IL‐1β‐treated chondrocytes. miR‐6779 inhibits XIAP expression, thereby promoting senescent chondrocyte cell apoptosis and reducing chondrocyte senescence and ECM loss through XIAP.

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