rHu MCP-1
- Known as:
- rHu MCP-1
- Catalog number:
- AK8196-0005
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Akro
- Gene target:
- rHu MCP-1
Related genes to: rHu MCP-1
- Gene:
- CCL2 NIH gene
- Name:
- C-C motif chemokine ligand 2
- Previous symbol:
- SCYA2
- Synonyms:
- MCP1, MCP-1, MCAF, SMC-CF, GDCF-2, HC11, MGC9434
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-05
- Date modifiied:
- 2016-10-05
- Gene:
- SLC25A14 NIH gene
- Name:
- solute carrier family 25 member 14
- Previous symbol:
- -
- Synonyms:
- BMCP1, UCP5
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-09
- Date modifiied:
- 2016-10-05
Related products to: rHu MCP-1
Related articles to: rHu MCP-1
- The sympathetic nervous system (SNS) plays a crucial role in chronic liver diseases, but its function, particularly in terms of the underlying mechanisms of liver metastasis, remains unclear. Here, we reported that hepatic sympathetic nerve activity increases in the early stage of metastasis and was accompanied by a moderate increase in norepinephrine (NE). Unexpectedly, NE had a dose-dependent effect on colorectal liver metastasis. Only daily administration of low-dose NE could maintain NE at a moderate concentration in the liver during this early phase significantly suppressed metastatic tumor growth. Conversely, extremely low NE concentrations (induced by 6-hydroxydopamine, 6-OHDA) or high-dose NE prompted liver metastasis. Single-cell RNA sequencing (scRNA-seq) demonstrated that NE modulated monocyte recruitment and M2 macrophage polarization through the CCL2-CCR2 signaling axis and influenced the immunosuppressive effects of myeloid-derived suppressor cells (MDSCs) on T cells: low-dose NE inhibited monocyte recruitment and M2 macrophage polarization and relieved the immunosuppressive effects of MDSCs on T cells, whereas extremely low- and high-dose NE supplementation had the opposite effects. Further investigations confirmed that these biological effects were closely associated with the NE-mediated expression ratio of α2a-adrenergic receptor to β2-adrenergic receptor (α2a-AR/β2-AR). Specifically, at moderate NE concentrations, a high α2a-AR/β2-AR expression ratio was correlated with antitumor effects. Collectively, these findings reveal that the SNS mediates U-shaped effects on liver metastasis in an α2a-AR/β2-AR ratio-dependent manner, highlighting moderate sympathetic activation as a potential therapeutic strategy to inhibit the progression of liver metastasis. - Source: PubMed
Publication date: 2026/06/23
Gao LuluLi JianLi BoruiHuang SonglinHu JiahongLiu ZhengDai YanfengLiu JinxinZhang RenWang JialuWang XinruLuo QingmingZhang Zhihong - Immunosuppression in ovarian cancer is primarily driven by myeloid-derived suppressor cells (MDSCs). This study identifies karyopherin α2 (KPNA2) as a novel regulator of this immunosuppressive process through the NF-κB/CCL2/CCR2 axis. Elevated KPNA2 expression correlates with increased intratumoral MDSC accumulation and impaired CD8 T-cell function. Mechanistically, KPNA2 directly binds to and facilitates nuclear translocation of NF-κB/p65, thereby driving CCL2 transcription, while also exhibiting an auxiliary, p65-independent function in CCL2 induction. Secreted CCL2 recruits MDSCs in a CCR2-dependent manner, establishing a potent immunosuppressive tumor microenvironment. Therapeutic targeting via MDSC depletion, pharmacological CCR2 blockade, or direct KPNA2 knockdown effectively inhibited metastasis, enhanced CD8+ T-cell infiltration, and suppressed tumor growth. Importantly, CCR2 inhibition synergized with anti-PD-L1 therapy, revealing a promising combination immunotherapeutic strategy for KPNA2-high ovarian cancer. These findings establish the KPNA2-governed NF-κB/CCL2/CCR2 pathway as a central mechanism of immune evasion and a viable target for combination immunotherapy in ovarian cancer. - Source: PubMed
Publication date: 2026/06/22
Li QingliZhao JitongYang LuLi LinBian CeYi TaoHuang HuiqiongZheng GangLin Xiaojuan - B7 family co-inhibitory molecules play a crucial role in maintaining homeostasis and preventing chronic inflammation. However, they also impede antitumor immune responses. Immunoglobulin-like domain-containing receptor 2 (ILDR2) is a B7 family member that modulates T cell activation. Previous studies demonstrated that its blockade synergizes with PD-L1 inhibition in mouse tumor models. Although ILDR2 likely contributes to immune evasion, the precise underlying mechanism remains unknown. Here, we investigated the effect of ILDR2 on the tumor microenvironment (TME) in a mouse squamous cell carcinoma (SCCVII) model. We generated ILDR2-expressing SCCVII cells (ILDR2-SCCVII) through transduction of the extracellular and transmembrane domains of ILDR2. Compared to control vector-transduced cells (Cont-SCCVII), ILDR2-SCCVII cells resulted in accelerated tumor growth and a reduced ratio of activated T cells in the TME 21 days after inoculation. At this late stage, most tumor-infiltrating leukocytes were Ly6C- F4/80 CD206 M2-like macrophages. Interestingly, at an earlier time point, we observed the increased infiltration of Ly6C F4/80/ monocytes-potential macrophage precursors-in ILDR2-SCCVII tumors. Whereas CCL2 expression was enhanced early after inoculation in both groups, its receptor CCR2 was more highly expressed on Ly6C F4/80/ monocytes specifically in the ILDR2-SCCVII group. Using our in-house anti-mILDR2 monoclonal antibody and ILDR2-Ig, we found that early recruited myeloid cells preferentially expressed ILDR2 and exhibited ILDR2-Ig binding. These results suggest that tumor-expressing ILDR2 interacts with myeloid cells during the early stages of tumor development, inducing premature monocyte accumulation via the CCL2-CCR2 axis. This early shift toward an M2 macrophage-mediated immunosuppressive environment likely accelerates tumor growth. - Source: PubMed
Publication date: 2026/06/20
Nagatomo YutoZhang ChenyangLu YiWidyagarini AmritaNagai Shigenori - Lung cancer remains a major challenge in clinical treatment, as current therapeutic strategies often fail to effectively halt disease progression. Chronic intermittent hypoxia (CIH), a hallmark pathological feature of obstructive sleep apnea (OSA), has been implicated in promoting tumor invasion and metastasis. This study aimed to investigate the potential of hydrogen as an innovative adjunctive therapy for lung cancer. To evaluate the therapeutic effects of hydrogen, both in vitro and in vivo models were established. In vitro, an intermittent hypoxia (IH) tumor cell-macrophage co-culture system was used to assess cell proliferation, migration, and macrophage polarization. In vivo, tumor growth was monitored in a CIH mouse model, and tissue samples were subsequently analyzed via immunohistochemistry and western blot. Our results demonstrated that hydrogen exerted significant antitumor effects in vivo. Mechanistically, this effect was associated with a shift in macrophage polarization toward the pro-inflammatory M1 phenotype and suppression of the CCL2-CCR2 signaling axis. In addition, in vitro studies revealed that hydrogen directly inhibited lung cancer cell survival and migration, and downregulated key components of the CCL2-CCR2 pathway, mirroring the effects observed with a CCR2 inhibitor. These findings highlighted that hydrogen treatment suppressed tumor growth by modulating the tumor immune microenvironment and inhibiting angiogenesis. Collectively, our results suggested that hydrogen may represented a novel and promising therapeutic strategy for lung cancer. - Source: PubMed
Publication date: 2026/06/20
Liu Qing-QingZhao Chen-BingWang ZhuoSun MengfangQi Ke-RongLiu HanLi QianZhao YashuoGuo Ya-JingJi En-Sheng - Doxorubicin (Doxo) is a DNA-damaging chemotherapeutic widely used in breast cancer (BC) treatment. While effective at inhibiting tumor cell proliferation, Doxo paradoxically enhances pro-inflammatory signaling between stromal and BC cells and promotes pro-migratory and invasive phenotypes. Identifying strategies to counteract these adverse effects remains a relevant therapeutic challenge. In this study, we synthesized a series of juglone (5-hydroxy-1,4-naphthoquinone) derivatives and evaluated their effects on mitochondrial bioenergetics and NAD(P)H Quinone Dehydrogenase 1 (NQO1)-dependent viability in BC cell lines (ZR75-1, MCF7, and MDA-MB-231) and RMF621 fibroblasts. Among these compounds, J2 (Cpd. J2) emerged as a selective inhibitor of proliferation, inducing S-phase cell cycle arrest and suppressing clonogenic capacity. In ZR75-1 and MCF7 cells, Cpd. J2 increased mitochondrial NADH levels. This effect was abolished by inhibitors of mitochondrial complex I, transaminases, and α-ketoglutarate/pyruvate dehydrogenases, indicating activation of the tricarboxylic acid cycle. Consistently, Cpd. J2 enhanced mitochondrial oxygen consumption rate and superoxide production. These metabolic effects were absent in MCF7 ρ0 cells, demonstrating a strict dependence on functional mitochondria. Moreover, Cpd. J2 significantly reduced Doxo-induced CCL2 secretion in RMF621 fibroblasts and inhibited the motility of low-migratory BC cells stimulated with conditioned medium from Doxo-treated fibroblasts. Mechanistically, Cpd. J2 decreased the Doxo-induced metabolic remodeling and increase in mct4, but not glut1, in RMF621 cells, and attenuated the upregulation of ccr2 and snail in MCF7 cells. Collectively, these data indicate that Cpd. J2 modulates mitochondrial redox balance via NQO1, inhibiting BC cell proliferation and disrupting Doxo-driven pro-migratory stromal-tumor signaling. - Source: PubMed
Publication date: 2026/06/19
Rodríguez-Lucart Yarcely AContreras-Saá IgnacioOlguín Camila FVera María JesúsMonroy-Cárdenas MatíasAlmarza CristopherTapia GladysPulgar RodrigoMartínez JorgeCaballero JulioAraya-Maturana RamiroUrra Felix A