Ask about this productRelated genes to: Stk25 antibody
- Gene:
- STK25 NIH gene
- Name:
- serine/threonine kinase 25
- Previous symbol:
- -
- Synonyms:
- SOK1, YSK1
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-18
- Date modifiied:
- 2014-11-19
Related products to: Stk25 antibody
Related articles to: Stk25 antibody
- Colon adenocarcinoma (COAD) remains a leading cause of cancer-related mortality worldwide. Although programmed cell death (PCD) and RNA N6-methyladenosine (m6A) modification have each been shown to regulate tumor progression and therapeutic responses, their combined prognostic significance in COAD has not been fully elucidated. The present study aimed to develop an integrated m6A-PCD prognostic model and to identify potential therapeutic targets in COAD. In total, 1,379 genes across 14 PCD-related pathways were systematically analyzed and a 21-gene m6A-PCD signature (MCDI) was constructed following multivariate Cox regression analysis. Single-cell RNA sequencing from publicly available datasets (GSE132465 and GSE205506), together with reverse transcription-quantitative PCR (qPCR) validation using clinical samples, were employed to identify genes with tumor-specific expression patterns. The functional role of serine/threonine kinase 25 (STK25) was further investigated through knockdown experiments, flow cytometry, m6A methylated RNA immunoprecipitation (MeRIP)-qPCR and RIP assays. In addition, small interfering RNAs targeting methyltransferase-like 3 (METTL3) and YTH domain-containing protein 1 (YTHDC1) were used to evaluate the involvement of m6A modification in STK25 mRNA stability and apoptosis regulation. The resulting MCDI signature demonstrated robust and independent prognostic value and effectively predicted differential responses to programmed death-ligand 1 immunotherapy. In total, 5 core genes [microRNA 210, STK25, TGFB2, tripartite motif containing (TRIM)6 and TRIM68] were identified as key prognostic markers. STK25 was specifically upregulated in tumor epithelial cells, and its knockdown significantly promoted apoptosis in COAD cells. Correlation analyses revealed positive associations between STK25 expression and multiple m6A regulators, with METTL3 and YTHDC1 showing the highest targeting credibility. Knockdown of METTL3 or YTHDC1 reduced STK25 mRNA levels. RIP assays confirmed their direct binding to STK25 mRNA, while MeRIP-qPCR demonstrated that METTL3 knockdown decreased the m6A modification level of STK25 mRNA. In conclusion, the reconstructed MCDI was established as a novel m6A-PCD-based prognostic model for patient stratification and the prediction of immunotherapy response in patients with COAD. STK25 was also identified as a potential therapeutic target linking m6A modification to the regulation of apoptosis in COAD. - Source: PubMed
Publication date: 2026/04/22
Yu HezhiLi TihuiHuang XiaoyunChen ZihanLin ZixiangChen Fenglin - Cancer-associated fibroblasts (CAFs) within the tumour microenvironment play a pivotal role in colorectal cancer (CRC) progression and therapeutic resistance. Serine/threonine protein kinase 25 (STK25) exerts multiple roles in tumourigenesis; however, its role in mediating tumour-stroma crosstalk remains largely unexplored. - Source: PubMed
Hou YifanChen JiangboHao HaoSong TongkunSong LinXing PuWeng KaiRan YumengYang XinyingQiao XiaowenChen JieYao RuibinYang HongChen LeiDi JiaboXu KaiSu XiangqianJiang Beihai - Atherosclerosis represents a chronic inflammatory disease of the arterial wall and remains a principal cause of cardiovascular morbidity and mortality. Macrophages critically govern lesion initiation, progression, and destabilization, and accumulating evidence indicates that protein kinases are key regulators of their phenotype and function. This systematic review synthesizes data from 162 publications encompassing 76 kinases to delineate the contribution of macrophage-associated kinase signaling to atherogenesis. The identified kinases span major families, including AGC, CaMK, CMGC, Ste20, and tyrosine kinases, each exerting distinct regulatory effects on macrophage survival, polarization, lipid handling, efferocytosis, and inflammatory activation. Several kinases, such as CaMK2γ, CaMK4, DCLK1, Trib1, and STK25, exhibit pro-atherogenic activity by promoting foam cell formation, expanding the necrotic core, and propagating inflammatory pathways. Conversely, kinases, including STK11 and the context-dependent mediator Akt1, exhibit protective or dual functions that contribute to metabolic homeostasis and reparative macrophage states. Despite substantial mechanistic insights and the established therapeutic utility of kinase inhibitors in oncology, clinical translation in the context of atherosclerosis remains limited. This review consolidates current knowledge, identifies critical gaps, and outlines prospective avenues to target macrophage-specific kinase pathways as novel therapeutic strategies for atherosclerosis. - Source: PubMed
Publication date: 2026/03/27
Müller Jana Svan der Vorst Emiel P C - Colorectal cancer (CRC) is a leading cause of cancer death, and the incidence and mortality rates among young adults are rising. Although a subset of CRC cases presents with a family history, suggesting a hereditary component, the specific genetic underpinnings remain incompletely understood, particularly in early-onset CRC (EOCRC). This study aimed to discover novel risk genes for EOCRC using exome sequencing and gene-based rare variant burden testing. Our cohort consisted of 212 European-ancestry cases (174 diagnosed with CRC and 38 with significant polyps) from the South Australian Young Onset Colorectal Polyp and Cancer Study (SAYO) and 31,699 unaffected controls from the Simons Foundation Powering Autism Research for Knowledge (SPARK) cohort. After filtering for ancestry, relatedness, variant quality, and population allele frequency, we performed gene-set and individual-gene burden tests using predicted deleterious missense and loss-of-function variants. Statistical significance was assessed using permutation-corrected binomial testing. An independent validation was conducted in the UK Biobank. Loss-of-function variants in known CRC tumor suppressor genes were significantly enriched in SAYO cases. Gene-level analyses identified as a novel EOCRC susceptibility candidate ( value = 1.0 × 10), with supporting enrichment of deleterious missense and loss-of-function variants in distal colon cancer cases from the UK Biobank. Additional genes (, , , , , and ) demonstrated borderline significance, implicating pathways related to kinetochore assembly, autophagy regulation, and immune signaling. Both predicted gain-of-function and loss-of-function variants contributed to the EOCRC risk, supporting heterogeneous mechanisms of CRC pathogenesis. This study identified novel candidate risk genes for EOCRC, underscoring the role of rare variants and expanding our understanding of the genetic architecture of CRC. Future studies should include functional validation and replication studies on other ancestries to confirm and extend these results. - Source: PubMed
Publication date: 2025/12/09
Song RuocenMikaeel Reger RHe ZhongpingHorsnell MehganUylaki WendyMeng WeiminPoplawski Nicola KWollnik BerndLi YunFeng JinghuaScott Hamish SShen YufengWang ChenYin RuiDing YousongLlor XavierChung Wendy KSmith EricPrice Timothy JYoung Joanne PFan Xiao - Obesity has reached pandemic proportions, highlighting the urgent need for continued research to uncover the molecular mechanisms governing lipid homeostasis and ectopic fat deposition in overnutrition. Our recent translational studies demonstrated that STE20-type kinases STK25 and MST3 associate with intracellular lipid droplets and play a pivotal role in regulating the dynamic balance between fat storage and utilization. This study aimed to assess the in vivo effects of the combined inhibition of STK25 and MST3 in obese mice. - Source: PubMed
Publication date: 2025/09/22
Andersson EmmaGongye XiangdongCansby EmmelieZhang JingjingCaputo MaraAsiedu BerniceGarellick ViktorBooten SheriMurray SueFont-Gironès FerranRuud JohanLind Dan EmilAmrutkar ManojHowell Brian WWernstedt Asterholm IngridMahlapuu Margit