Ask about this productRelated genes to: IL24 antibody
- Gene:
- IL24 NIH gene
- Name:
- interleukin 24
- Previous symbol:
- ST16
- Synonyms:
- mda-7, IL10B, Mob-5, C49A, FISP, IL-24
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-02
- Date modifiied:
- 2016-10-05
Related products to: IL24 antibody
Related articles to: IL24 antibody
- Cancer terminator viruses (CTVs) are next‑generation conditionally replicating oncolytic adenoviruses that integrate precise tumor targeting, direct oncolysis, and potent cytokine‑mediated immunotherapy into a single platform. In CTVs, viral replication is driven by cancer‑selective promoters such as the progression elevated gene‑3 (PEG‑3) promoter, restricting E1A expression and adenoviral replication to tumor cells while sparing normal tissues. These vectors are "armed" with broad‑acting immunomodulatory cytokines, most notably melanoma differentiation-associated gene‑7/interleukin‑24 (mda‑7/IL‑24) or interferon‑gamma, which can induce cancer‑selective apoptosis, toxic autophagy, anti‑angiogenesis, and robust innate and adaptive immune responses, including "bystander killing" of distant, noninfected tumor cells. Chimeric fiber‑modified backbones such as Ad.5/3 enhance infection of Coxsackie-adenovirus receptor-deficient tumors, broadening applicability to refractory epithelial, prostate, brain, and pancreatic cancers. Preclinical studies demonstrate that CTVs eradicate primary and metastatic lesions in multiple xenograft models and synergize with chemotherapy, radiotherapy, and immune checkpoint inhibitors, especially when combined with advanced delivery technologies such as ultrasound‑targeted microbubble destruction and focused ultrasound double-microbubble platforms for systemic, site‑directed release. Ongoing efforts to incorporate IL‑24 "Superkine," fusion cytokines and fusion Superkines, and rational combinations with immunotherapies position CTVs as a versatile and clinically translatable viro-immunotherapeutic strategy for advanced solid tumors. Progress in these efforts will pave the way for applying these virotherapies for improved cancer treatments in the clinic. - Source: PubMed
Publication date: 2026/04/16
Roy Pritam KumarMir Shahid MaqboolMamidi NarsimhaMannangatti PadmanabhanGammel TheresaLimbrick David DSarkar DevanandDas Swadesh KFisher Paul B - We investigated the role of GLI3, a transcription factor highly expressed in the pathogenic THY1CD34 sublining subset of rheumatoid arthritis synovial fibroblasts (RASFs), in regulating their pathogenic behavior. - Source: PubMed
Sato MotohikoSaito TetsuyaKomiya YojiNoda SeijiTagawa YasuhiroYamamoto AkioIwai HideyukiEndo KentaroKoga HideyukiTakahara YasuhiroSugimoto KazutakaSekiya IchiroKawakami EiryoHosoya TadashiYasuda Shinsuke - An overactivated cytokine storm during the early phase of sepsis is associated with increased mortality. Although various cytokine-targeting therapeutic strategies have been evaluated in clinical trials, their efficacy remains limited. Here, we focus on the previously less studied cytokine interleukin-24 (IL-24) and demonstrate its pathogenic role in ()-induced sepsis. Elevated IL-24 expression was observed in septic wild-type mice. In contrast, IL-24 knockout mice exhibited improved survival, reduced bacterial load, and diminished neutrophil and T-cell infiltration. Both and experiments revealed that recombinant IL-24 protein enhances the bacterial accumulation and leukocyte chemotaxis. Finally, inhibition of IL-24 expression significantly reduced sepsis-associated mortality. These findings suggest that IL-24 contributes to sepsis pathogenesis by promoting bacterial dissemination and inflammatory amplification, and identify IL-24 as a potential therapeutic target for the precise treatment of sepsis. - Source: PubMed
Publication date: 2026/06/02
Lu JinjinLiao YuanLiu ZhongshuangHe JiankangXie WenqiangShen Yuqin - mRNA-based therapeutics offer significant potential for cancer treatment owing to their ability to induce transient, non-integrating expression of therapeutic proteins. However, effective and tumour-specific delivery remains a major barrier. In this study, we report a cell membrane vesicle (CMV)-based delivery platform for targeted mRNA therapy, employing engineered CMVs enriched with the surface molecule CD6 for the selective delivery of Il24 mRNA to CD166-overexpressing tumour cells. CMVs were derived from NIH-3T3 cells via cytochalasin B induction and genetically modified to express CD6, enabling biomimetic targeting through the CD6-CD166 axis. Il24 mRNA was loaded into CD6-CMVs through a digitonin-assisted permeabilisation strategy, achieving high encapsulation efficiency and sustained intracellular release. In vitro, CD6-CMVs facilitated enhanced uptake in CT26 cells, leading to elevated IL-24 expression, activation of apoptotic and autophagic pathways, and suppression of migration and invasion. In mouse colorectal cancer and squamous carcinoma models, CD6-CMVs/Il24 mRNA demonstrated effective tumour targeting, increased intratumoral IL-24 translation, and potent antitumor efficacy, with minimal off-target accumulation or systemic toxicity. Notably, this treatment promoted immune cell infiltration and reshaped the tumour microenvironment towards a pro-inflammatory state. This study presents a scalable, low-immunogenicity CMV platform capable of targeted mRNA delivery and cytokine expression, offering a promising strategy for precision immunotherapy for solid tumours. - Source: PubMed
Wang DandanGao RuofanLiu DuoLi KefanWang RunkaiXu MingheZhang ShiweiJiang ShengjieXia Bin - Cabazitaxel is a second-generation semisynthetic taxane approved for the treatment of prostate cancer. Vitamin K, an essential nutrient involved in blood coagulation and bone metabolism, has also been shown to have antineoplastic effects. However, no information is currently available regarding the combinatorial effects of cabazitaxel and menadione (VK3, a derivative of vitamin K) on prostate cancer cells. Therefore, we investigated the in vitro effects of cabazitaxel, VK3, and their combination on growth, mitochondrial bioenergetics, and glycolytic parameters using the human prostate cancer cell lines PC-3 and DU 145. All treatments inhibited the cell growth, but the combination of cabazitaxel and VK3 produced a synergistic effect that was stronger than either compound alone, and these effects were accompanied by cell line-specific bioenergetic changes and glycolytic responses. Furthermore, high-throughput transcriptomic profiling of PC-3 cells revealed distinct sets of differentially expressed genes for each treatment, with the greatest effect established by the combinatorial treatment, followed by VK3, and then cabazitaxel. Gene ontology analyses showed that the combinatorial treatment was associated with biological processes such as positive regulation of reactive oxygen species metabolic process, steroid metabolic process, proteolysis, and signal transduction. Notably, the treatments altered the gene expression of several tumorigenic and immunologic mediators, including , , , , and , which may impact cancer cell behavior. In conclusion, these in vitro findings indicate that the combination of cabazitaxel with VK3 is more effective in inhibiting prostate cancer cell growth than either agent alone and provide exploratory mechanistic insight into their effects on cancer cell metabolism and gene expression. - Source: PubMed
Publication date: 2026/05/17
Gómez-Rosas Ana LauraChirinos MayelNoyola-Martínez NancySegovia-Mendoza MarianaTorres-Ramírez NayeliRomero-Córdoba SandraNoriega Lilia GGarcía-Olivares MitziLarrea FernandoBarrera David