Ask about this productRelated genes to: KRT23 antibody
- Gene:
- KRT23 NIH gene
- Name:
- keratin 23
- Previous symbol:
- -
- Synonyms:
- K23, DKFZP434G032, HAIK1, CK23, MGC26158
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2016-03-09
Related products to: KRT23 antibody
Related articles to: KRT23 antibody
- Sepsis is a persistent systemic inflammatory disease involving multiple organ failure caused by a dysregulated immune response to infection. As primary effector cells in innate immunity, neutrophils significantly contribute to combating infections and mediating inflammatory responses. The aim of this study was to evaluate the prognostic significance of neutrophil-related genes (NRGs) in sepsis and their relationship with the immune microenvironment. - Source: PubMed
Publication date: 2025/12/11
Sun FanShi MinLi XiaodongLiu XueyunWang Xiaowei - Colorectal cancer (CRC) represented a pervasive manifestation of malignant neoplasia within the digestive tract. Apigenin, exhibiting a multitude of physiological attributes and pharmacological actions, has undergone extensive scrutiny for its antitumor efficacy and benign toxicity profile. Cisplatin (DDP)-centered chemotherapy constituted a pivotal aspect of multidisciplinary therapeutic strategies. Nevertheless, resistance to DDP posed a considerable impediment to the efficacy of CRC chemotherapy. The aim of this investigation was to assess the impact of combining Apigenin with DDP on the proliferation and apoptotic processes of human CRC cells, while also delving into the underlying mechanisms. HCT116 and SW480 were cultivated and subjected to treatment with Apigenin (API) either as a monotherapy or in combination with cisplatin (DDP). Cell viability, proliferation, cycle distribution, apoptosis, migration, invasion and inflammatory factors were assessed. Western blot analysis was performed to detect the protein expression levels of Glut1, HK-2, KRT23, and β-catenin. In comparison to other treatment groups, the combined API and DDP group exhibited a more potent suppressive effect on cellular proliferation, migration, invasion, and glycolysis, while also enhancing apoptotic activity. Additionally, the combined API and DDP treatment group led to a reduction in the expression levels of KRT23, β-catenin, HK-2, and Glut1. Intriguingly, this combined treatment group demonstrated significantly elevated levels of TNF-α, IL-6, and IL-8 compared to the other groups. Notably, the overexpression of KRT23 was capable of reversing the changes induced by the combined API and DDP treatment. In vivo studies further validated that the combined API and DDP treatment suppressed tumor growth by inhibiting the expression of KRT23 and β-catenin. The present findings indicated that the combination of API with DDP has the potential to enhance colorectal cancer therapy through the modulation of the KRT23/Wnt/β-catenin signaling pathway. Our research may offer fresh perspectives and novel molecular therapeutic strategies for the treatment of colorectal cancer. - Source: PubMed
Publication date: 2025/11/28
Dong LeiYang FengWang XueZhang WeiSong JucaiJiao PanpanKang MengjieGuo QianqianSi LiangzhuZhang ShuhanHuang MeiLuo LinshanLi YongweiGong Yuesheng - Could cephalosporin antibiotics, extending beyond their established antimicrobial role, be repurposed as precision anticancer agents and chemosensitizers, particularly against inflammation-driven carcinogenesis? To address this question, this study systematically evaluated the anti-colorectal cancer efficacy of cephalosporins both as monotherapies and in synergistic combinations, elucidating their underlying molecular mechanisms. Employing combinatorial phenotypic screening (viability, cell cycle, apoptosis, colony formation), BALB/c nude mouse xenografts, and omics profiling (RNA-seq, RT-qPCR), we identified conserved anticancer pathways and core regulatory axes. Among 18 evaluated cephalosporins, therapeutic specificity was largely associated exclusively variable side-chain moieties, not the conserved β-lactam core. Cefamandole nafate (CAN) and cefuroxime sodium (CUS) demonstrated potent dual efficacy against colorectal cancer model while enhancing cisplatin chemosensitivity. Building on links to inflammation-driven chemosensitization, CUS synergistically potentiated cisplatin and levofloxacin cytotoxicity in colorectal cancer. This synergy was mechanistically driven by apoptosis induction, cell cycle arrest, significant up-regulation of HMOX1 (80-fold peak in combinations; 40-fold as monotherapy) and DDIT3, coupled with down-regulation of MUC1, CASC19, KRT23, SPNS3, LFNG, HS3ST1, NCOA5, and GJB4. Crucially, we reveal for the first time that CUS significantly up-regulates HMOX1 expression in HCT116 cells in a dose-dependent manner, establishing this ferroptosis regulator as the central effector governing both intrinsic anticancer activity and chemosensitization. This study unveils the translational potential of repurposing cephalosporins for combinatorial precision oncology strategies targeting inflammation-driven cancers. - Source: PubMed
Publication date: 2025/11/21
Liu NianqiuCao WeihanTang JiefuDong RuimeiGuo JuanLuo ZhuangYao QianTeng SongLiang ZhuoxuanYang YuntaoGu MenyingZhou JieChen WenlinLiang HongminHe Xiaoqiong - Gastric cancer (GC) is a highly prevalent and lethal malignancy worldwide. Notwithstanding advances in treatment, suboptimal patient outcomes highlight the urgent need for novel therapeutic targets to improve survival. This study aimed to explore the influence of keratin 23 (KRT23) on the proliferation, migration, and invasion of GC cells, as well as its underlying molecular mechanism. - Source: PubMed
Publication date: 2025/10/29
Xie YiZhou FanghuiLi XuelianPeng Pailan - It is urgent to explore the potential biomarkers for pancreatic cancer (PC) prognosis and treatment to improve patients' outcomes. - Source: PubMed
Publication date: 2025/10/07
Cui ZhongyuanLei XiaGou YaniWu ZhixianHuang Xiaojun