Ask about this productRelated genes to: CXCL16 protein
- Gene:
- CXCL16 NIH gene
- Name:
- C-X-C motif chemokine ligand 16
- Previous symbol:
- -
- Synonyms:
- SR-PSOX, CXCLG16, SRPSOX
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-21
- Date modifiied:
- 2016-10-05
Related products to: CXCL16 protein
Related articles to: CXCL16 protein
- Tumor-associated macrophages (TAMs) are pivotal in the immunosuppressive tumor microenvironment of pancreatic ductal adenocarcinoma (PDAC). The efficacy of targeting the CSF-1/CSF-1R axis in PDAC remains uncertain. Using single-cell RNA sequencing on specimens from patients treated with Surufatinib plus chemotherapy, we identified a distinct subset of damage-associated macrophages (DAMs) characterized by high GPR34 expression. In Gpr34 mouse models and in vitro co-cultures, GPR34 macrophages responded to tissue damage by releasing lysophosphatidylserine (LysoPS), which enhanced CXCL16 secretion and efferocytosis. This efferocytosis promoted MHC-I degradation via the macrophage lysosomal pathway, leading to CD8 T cell exhaustion. Combining a GPR34 antagonist with chemotherapy and surufatinib significantly enhanced anti-tumor responses in preclinical models. These findings identify GPR34 as a promising immune therapeutic target. - Source: PubMed
Publication date: 2026/04/28
Guo XiaofanLiu YuxiaoLi TianchenAn XiaopengSong YuningXu PeijunHuang JingZou YipingXu BohangXie YongjieLi ZekunMeng ChenyangZhao TiansuoWang XiuchaoWang HongweiGao ChuntaoZhou XuanYu JunGao SongHao Jihui - Endothelial dysfunction profoundly compromises the barrier function that precludes trans-endothelial entry of low-density lipoprotein cholesterol (LDL-C) into the vessel wall. LDL-C retention in the vessel wall is atherogenic and its flux involves several mechanisms including LDL-receptor (LDL-R) mediated transcytosis, a process that is facilitated by inflammatory stressors. In this study, we aimed to investigate the role of interleukin-6 (IL-6) in regulating LDL-R and LDL-C uptake by vascular endothelial cells. - Source: PubMed
Publication date: 2026/04/25
Zegeye Mulugeta MVeettil Jishamol TParamel Geena VKurt SetaSalihovic SamiraLjungberg Liza UKumawat Ashok KSirsjö Allan - Breast cancer is the foremost cause of cancer-related death in women globally, and taxane-anthracycline (TA) combination regimens represent standard frontline chemotherapy. Although widely administered, the pathological complete response rate to TA therapy is less than 30%, and chemoresistance remains a major barrier to effective disease control, frequently leading to relapse and poor survival. Both metabolic reprogramming and tumor microenvironmental remodeling are closely associated with treatment failure, yet how they interact to drive TA resistance remains largely unclear. Here we show that phosphofructokinase platelet (PFKP), a key glycolytic enzyme, is highly expressed in breast cancer. PFKP drives glycolysis and promotes CD133 cancer stem-like cells (CSLCs) that are inherently TA-resistant. Moreover, PFKP-overexpressing cancer cells stimulate cancer-associated fibroblasts (CAFs), which in turn augment CD133 CSLC formation via the CXCL16/CXCR6 axis, establishing a feedforward loop that reinforces chemoresistance. These results reveal a previously unappreciated mechanism by which a glycolytic enzyme in cancer cells orchestrates stromal crosstalk to sustain a chemotherapy-refractory niche. By identifying PFKP as a key driver and the PFKP-CSLC-CAF axis as an actionable target, our work moves the field beyond the traditional view of metabolic reprogramming as a cell-autonomous event. Disrupting this axis-for instance, by PFKP inhibition or CXCL16/CXCR6 blockade-may restore TA sensitivity in aggressive basal-type breast cancer, offering a promising strategy to improve long-term outcomes for hard-to-treat patients. - Source: PubMed
Publication date: 2026/04/23
Fang KaiMa YueLi LihuaYue YanRuan HangXiong Sidong - Hypertension is a major modifiable risk factor for chronic kidney disease (CKD), yet predicting which hypertensive individuals will progress to CKD remains challenging. We aimed to develop and validate a plasma protein-based risk score for incident CKD in hypertension and to identify causal proteins and potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/22
Huang YuChen DanYe ZiliangZhang YanjunYang SisiGan XiaoqinZhang YiweiWu YitingZhang YuanyuanQin Xianhui - The heterogeneity in health effects of circulating proteins remained unclear. Previous studies have identified that glycoprotein acetyls (GlycA), a stable biomarker of inflammation, were associated with risks of mortality and chronic diseases. However, it remained unclear whether the health risks of proteins may differ across people with varied GlycA levels. Based on the multi-omics profiling of the UK Biobank prospective cohort, we evaluated whether GlycA statistically modifies the protein-mortality associations. In the discovery dataset (n = 24,134), we observed that GlycA significantly modified the associations of ANG, CRHBP, CXCL16, and PRRT3 with all-cause mortality, and these findings were replicated in the validation dataset (n = 6081). Subgroup analyses further indicated that associations between these proteins and mortality can be modulated by GlycA levels. Through exploratory analyses focused on chronic diseases and cause-specific mortality, we identified that cross-products of GlycA with these proteins can be associated with cancer mortality and heart failure. Together, the findings will expand our understanding of heterogeneity in protein-health associations and highlight several potential therapeutic targets for interventions across people with varied inflammation status. - Source: PubMed
Wang XinruQiao ZiyanTao ChengzheLiao SijingLi ZhiXu QiaoqiaoFan YunWang YufengHan YanDai XiuliangLu Chuncheng