COLEC12 Pre-design Chimera RNAi
- Known as:
- COLEC12 Pre-design Chimera RNAi
- Catalog number:
- H00081035-R04
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- COLEC12 Pre-design Chimera RNAi
Related genes to: COLEC12 Pre-design Chimera RNAi
- Gene:
- COLEC12 NIH gene
- Name:
- collectin subfamily member 12
- Previous symbol:
- -
- Synonyms:
- SRCL, CL-P1, SCARA4
- Chromosome:
- 18p11.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-13
- Date modifiied:
- 2015-11-16
Related products to: COLEC12 Pre-design Chimera RNAi
Related articles to: COLEC12 Pre-design Chimera RNAi
- Collectin Subfamily Member 12 (COLEC12), a C-type lectin family member with collagen-like and carbohydrate recognition domains, remains poorly characterized in pancreatic cancer (PC). COLEC12 expression was analyzed by bioinformatics and immunohistochemistry. Functional assays (CCK-8, colony formation, EdU, flow cytometry, Transwell) and a xenograft model were used to assess its tumor-promoting effects. Mechanistically, transcriptome sequencing, Western blotting, co-immunoprecipitation (Co-IP), molecular docking, truncation mutant mapping, cycloheximide (CHX) chase assay, and ubiquitination assays were performed. The Cancer Genome Atlas (TCGA) data were used for immune infiltration analysis, and quantitative real-time PCR (qRT-PCR) was used to examine the role of COLEC12 in macrophage polarization. Chemosensitivity to gemcitabine and 5-fluorouracil (5-FU) was also evaluated. COLEC12 was upregulated in PC and promoted cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while suppressing apoptosis. Mechanistically, COLEC12 directly bound to TGF-β1 via its collagen-like domain, as demonstrated using truncation mutants. CHX chase assays revealed that COLEC12 overexpression delayed TGF-β1 degradation, and ubiquitination assays showed that COLEC12 knockdown increased TGF-β1 ubiquitination, indicating that COLEC12 stabilizes TGF-β1 by suppressing its ubiquitin-proteasome degradation, thereby sustaining activation of the TGF-β/Smad pathway. Furthermore, COLEC12 expression positively correlated with immune cell infiltration levels in TCGA data, and qRT-PCR revealed that COLEC12 expression in PC cells promotes M2 polarization of co-cultured macrophages. Knockdown of COLEC12 increased the sensitivity of PC cells to gemcitabine and 5‑FU. This study reveals, for the first time, the tumor-promoting function of COLEC12 in PC and highlights its potential as a therapeutic target in PC. - Source: PubMed
Publication date: 2026/06/19
Feng XinXu JianYang QingqingRen YiChen HuizhuJiang Zheng - Lung cancer, especially small-cell lung cancer (SCLC), is a widespread and deadly disease often detected at advanced stages, resulting in low five-year survival rates. This study aims to identify new genetic targets to enhance understanding of the genetic drivers of SCLC progression. - Source: PubMed
Publication date: 2026/03/21
Liu HailinQu FangyuanZhou GuangyaoCui YuechenYan BoZhang LianminLi ChenguangZhang ZhenfaQin TingtingZhang Qiangzhe - Ovarian cancer (OC) progression and metastasis are promoted by ascites, which constitutes a central part of the tumor microenvironment (TME). In this fluid, tumor-associated macrophages (TAMs) represent a prominent immune cell type. In addition to tumor and other host cells such as TAMs, ascites is highly enriched in soluble factors as well as extracellular vesicles (EVs). How TAMs contribute to the EV compartment of the OC TME remains, however, underexplored. In this work peripheral blood monocytes from healthy donors were differentiated into monocyte-derived macrophages (MDMs) and polarized into classically activated (M1-like), alternatively activated (M2-like) and TAM-like (by ascites incubation). For all subtypes, serum-free conditioned medium was collected for 24 h and EVs were isolated and characterized by nano-flow cytometry (nFC), label-free mass spectrometry-based proteomics and electron microscopy, among others. Our results demonstrated distinct traits for EV release and cargo across the different macrophage subtypes. Specifically, TAM-like macrophages exhibited impaired release of small EVs and reduced frequency of tetraspanin-positive particles. These EV subpopulations displayed sizing profiles closer to M1-like than to M2-like samples. Also, the low EV release in TAM-like MDMs was accompanied by altered expression of biogenesis-related markers like flotillin-1 (FLOT1) and a decreased N-glycosylation of CD63 protein, which was validated in patient-derived samples. Remarkably, the EV-associated proteome of TAMs displayed significant enrichment in both pro- and anti-inflammatory molecules with clinical value. Markers significantly enriched in the ascites TAM-EV signature were mostly associated with poor prognosis, whereas M1-like EV-related markers (pro-inflammatory) were mostly associated with longer survival. Our results confirmed previous data for proteins like CD163 and MRC1 to be associated to TAM-EVs, while also describing novel candidates with diagnostic (i.e., COLEC12) and/or prognostic (i.e., MSR1) value in plasma. Taken together, our data support a unique secretory profile of TAMs in OC and provide new EV-associated biomarkers with translational impact. Our results pave the way for a better understanding of the mechanisms behind TAM-EV cargo loading and function, and how these cells participate in the TME landscape. - Source: PubMed
Publication date: 2026/01/30
Pörschke JohannaHeidemann SophieNehring Hannah PLluch AinaSzymański WitoldFinkernagel FlorianPreußer ChristianBhagwat Aditya MStamm Timm JSommerfeld LeahHelmprobst FrederikMüller RolfReinartz SilkeGraumann JohannesPogge von Strandmann ElkeGómez-Serrano María - While optimal fluoride (F) levels support oral health, chronic exposure to high concentrations can lead to skeletal and dental fluorosis, especially in children. Emerging evidence suggests that excessive fluoride intake may disrupt systemic physiology, yet the underlying mechanisms remain poorly understood. To address this gap, we performed a comparative urinary proteomic analysis using LC-MS/MS in schoolchildren residing in a high-fluoride region, categorizing participants into high-fluoride (HF) and low-fluoride (LF) groups based on urinary fluoride excretion. Among 460 quantified proteins, ten were differentially expressed in the HF group, six upregulated (PHPT1, SPP1, COLEC12, CST4, DCHS1, LDHB) and four downregulated (CTSH, NECTIN1, TNC, KLK1). Gene Ontology enrichment highlighted associations with cell adhesion, ossification, and tissue development. Notably marked alterations in osteopontin (SPP1) and tenascin-C (TNC), key regulators of bone remodeling and dental matrix organization, suggesting disrupted focal adhesion signaling, impaired matrix integrity, and dysregulated biomineralization. Additional changes in proteins associated with enamel formation, oxidative stress, and immune regulation suggest that high fluoride exposure may broadly disrupt extracellular matrix organization and trigger inflammatory pathways. These findings demonstrate that excessive fluoride exposure induces systemic molecular disturbances in children, with implications for bone and soft tissue homeostasis. This research adds to the body of human evidence concerning fluoride's biological impact, advocating for vigilant exposure monitoring. - Source: PubMed
Publication date: 2026/01/06
Pongsapipatana NawapanGavila PatcharapornCho Sung-DaeEl-Tanani MohamedRabbani Syed ArmanIslam SofiqulEssigmann John MSriwattanapong KanokwanPorntaveetus Thantrira - Lenvatinib resistance remains a critical barrier in advanced hepatocellular carcinoma (HCC) therapy. However, the underlying mechanisms and strategies for reversing resistance remain incompletely understood. - Source: PubMed
Publication date: 2026/01/20
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