Ask about this productRelated genes to: KCTD21 antibody
- Gene:
- KCTD21 NIH gene
- Name:
- potassium channel tetramerization domain containing 21
- Previous symbol:
- -
- Synonyms:
- KCASH2
- Chromosome:
- 11q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-07-03
- Date modifiied:
- 2015-08-25
Related products to: KCTD21 antibody
Related articles to: KCTD21 antibody
- BACKGROUND: Immune checkpoint inhibitors (ICIs) have improved outcomes for patients with non-small cell lung cancer (NSCLC), yet their efficacy is hindered by the immunosuppressive and therapy-resistant tumor immune microenvironment (TIME). Long non-coding RNAs (lncRNAs) have emerged as critical regulators of immune signaling, ferroptosis, and cellular interactions within the TIME, highlighting their potential roles in shaping ICI response. MAIN BODY: LncRNAs modulate multiple layers of antitumor immunity in NSCLC. They regulate immune evasion through PD-1/PD-L1 signaling (SNHG12, SChLAP1, PCAT1, NEAT1), influence T-cell survival and differentiation (NKILA, MIR17HG), and affect macrophage phagocytic checkpoints (KCTD21–AS1–CD47). LncRNAs also integrate ferroptosis, stemness, and metabolic rewiring, as exemplified by RGMB-AS1 and AC026356.1. Several lncRNAs—including ADAMTS9–AS2, PCBP1–AS1, LY6K-AS, FAM207BP, and LINC01833—exhibit prognostic or predictive significance for immunotherapy. Exosomal lncRNAs further offer minimally invasive tools for liquid biopsy and longitudinal monitoring. Translational opportunities include nucleic acid therapeutics, innovative delivery systems, and rational combinations of ICIs with ferroptosis inducers or metabolic modulators. Multi-omics and spatial transcriptomics are essential to clarify mechanisms and identify high-confidence clinical candidates. CONCLUSIONS: LncRNAs are central regulators of NSCLC antitumor immunity and determinants of ICI sensitivity. Their dual potential as biomarkers and therapeutic targets underscores the need for mechanistic validation, multi-omics integration, and prospective clinical trials to accelerate their translation into NSCLC immunotherapy. - Source: PubMed
Publication date: 2025/12/26
Wang WeiweiJiang ZhibiaoZhao KunTeng YuanyinWu LinglingYu TingShang Anquan - Ovarian cancer (OC) remains one of the most lethal gynecological malignancies, characterized by late-stage diagnosis and high recurrence rates. Despite advances in treatment, the overall survival rate for OC patients remains low due to the lack of reliable biomarkers for early detection and prognosis. Thus, there is an urgent need for novel diagnostic and prognostic biomarkers to improve patient outcomes. In this study, we explored the potential role of the KCTD (Potassium Channel Tetramerization Domain-containing) family genes in OC. - Source: PubMed
Zhang LingCheng ChongTang Bin - Blocking immune checkpoint CD47/SIRPα is a useful strategy to engineer macrophages for cancer immunotherapy. However, the roles of CD47-related noncoding RNA in regulating macrophage phagocytosis for lung cancer therapy remain unclear. This study aims to investigate the effects of long noncoding RNA (lncRNA) on the phagocytosis of macrophage via CD47 and the proliferation of non-small cell lung cancer (NSCLC) via TIPRL. Our results demonstrate that lncRNA KCTD21-AS1 increases in NSCLC tissues and is associated with poor survival of patients. KCTD21-AS1 and its m6A modification by Mettl14 promote NSCLC cell proliferation. miR-519d-5p gain suppresses the proliferation and metastasis of NSCLC cells by regulating CD47 and TIPRL. Through ceRNA with miR-519d-5p, KCTD21-AS1 regulates the expression of CD47 and TIPRL, which further regulates macrophage phagocytosis and cancer cell autophagy. Low miR-519d-5p in patients with NSCLC corresponds with poor survival. High TIPRL or CD47 levels in patients with NSCLC corresponds with poor survival. In conclusion, we demonstrate that KCTD21-AS1 and its m6A modification promote NSCLC cell proliferation, whereas miR-519d-5p inhibits this process by regulating CD47 and TIPRL expression, which further affects macrophage phagocytosis and cell autophagy. This study provides a strategy through miR-519-5p gain or KCTD21-AS1 depletion for NSCLC therapy by regulating CD47 and TIPRL. - Source: PubMed
Publication date: 2024/02/21
Liang Dong-MinLi You-JieZhang Jia-XiangShen Huan-HuanWu Chun-XiaXie NingLiang YanLi Yan-MeiXue Jiang-NanSun Hong-FangWang QinYang JianLi Xiao-HuaWang Ping-YuXie Shu-Yang - The Sonic Hedgehog (Hh) signal transduction pathway plays a critical role in many developmental processes and, when deregulated, may contribute to several cancers, including basal cell carcinoma, medulloblastoma, colorectal, prostate, and pancreatic cancer. In recent years, several Hh inhibitors have been developed, mainly acting on the Smo receptor. However, drug resistance due to Smo mutations or non-canonical Hh pathway activation highlights the need to identify further mechanisms of Hh pathway modulation. Among these, deacetylation of the Hh transcription factor Gli1 by the histone deacetylase HDAC1 increases Hh activity. On the other end, the KCASH family of oncosuppressors binds HDAC1, leading to its ubiquitination and subsequent proteasomal degradation, leaving Gli1 acetylated and not active. It was recently demonstrated that the potassium channel containing protein KCTD15 is able to interact with KCASH2 protein and stabilize it, enhancing its effect on HDAC1 and Hh pathway. KCTD15 and KCTD1 proteins share a high homology and are clustered in a specific KCTD subfamily. We characterize here KCTD1 role on the Hh pathway. Therefore, we demonstrated KCTD1 interaction with KCASH1 and KCASH2 proteins, and its role in their stabilization by reducing their ubiquitination and proteasome-mediated degradation. Consequently, KCTD1 expression reduces HDAC1 protein levels and Hh/Gli1 activity, inhibiting Hh dependent cell proliferation in Hh tumour cells. Furthermore, analysis of expression data on publicly available databases indicates that KCTD1 expression is reduced in Hh dependent MB samples, compared to normal cerebella, suggesting that KCTD1 may represent a new putative target for therapeutic approaches against Hh-dependent tumour. - Source: PubMed
Publication date: 2023/08/17
Di Fiore ABellardinelli SPirone LRusso RAngrisani ATerriaca GBowen MBordin FBesharat Z MCanettieri GFabretti FDi Gaetano SDi Marcotullio LPedone EMoretti MDe Smaele E - Although animal dispersal is known to play key roles in ecological and evolutionary processes such as colonization, population extinction and local adaptation, little is known about its genetic basis, particularly in vertebrates. Untapping the genetic basis of dispersal should deepen our understanding of how dispersal behaviour evolves, the molecular mechanisms that regulate it and link it to other phenotypic aspects in order to form the so-called dispersal syndromes. Here, we comprehensively combined quantitative genetics, genome-wide sequencing and transcriptome sequencing to investigate the genetic basis of natal dispersal in a known ecological and evolutionary model of vertebrate dispersal: the common lizard, Zootoca vivipara. Our study supports the heritability of dispersal in semi-natural populations, with less variation attributable to maternal and natal environment effects. In addition, we found an association between natal dispersal and both variation in the carbonic anhydrase (CA10) gene, and in the expression of several genes (TGFB2, SLC6A4, NOS1) involved in central nervous system functioning. These findings suggest that neurotransmitters (serotonin and nitric oxide) are involved in the regulation of dispersal and shaping dispersal syndromes. Several genes from the circadian clock (CRY2, KCTD21) were also differentially expressed between disperser and resident lizards, supporting that the circadian rhythm, known to be involved in long-distance migration in other taxa, might affect dispersal as well. Since neuronal and circadian pathways are relatively well conserved across vertebrates, our results are likely to be generalisable, and we therefore encourage future studies to further investigate the role of these pathways in shaping dispersal in vertebrates. - Source: PubMed
Publication date: 2023/03/26
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