HOXA10 antibody
- Known as:
- HOXA10 (anti-)
- Catalog number:
- orb28152
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- HOXA10 antibody
Related genes to: HOXA10 antibody
- Gene:
- HOXA10 NIH gene
- Name:
- homeobox A10
- Previous symbol:
- HOX1H, HOX1
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2015-08-25
Related products to: HOXA10 antibody
Related articles to: HOXA10 antibody
- Radiation-induced intestinal injury (RIII) represents a significant dose-limiting complication of radiotherapy, characterized by substantial loss of intestinal epithelial cells (IECs). While the activation of cannabinoid receptor 2 (CB2R) is protective in immune‑mediated colitis, the intrinsic role of CB2R in IECs and its potential therapeutic relevance in RIII have not been defined. - Source: PubMed
Publication date: 2026/05/16
Yao QianyiTian YingYuan YiCai YongqingYang QunfangZhang LanfangLi YunongWei TanjunWang YiOuyang QinZhang HaigangLi XiaoliLiu Tao - : Aging is increasingly recognized as a key determinant of changes in human tissue and cellular function. Women's age, in particular, has been associated with reduced oocyte quality and negatively correlated with the expression of genes involved in endometrial decidualization and cellular function. The ability of endometrial cells to interact and allow the invasion of the growing embryo is defined as endometrial receptivity. Investigating age-related differences in human endometrial receptivity may expand our understanding of factors contributing to infertility. : Stromal cells were isolated and cultured from endometrial pipelle biopsies ( = 28) obtained from female donors at the proliferative phase of the menstrual cycle. Protein and mRNA expression of the receptivity modulators OPN, CD44, and HOXA10 were analyzed by Western blot and real-time PCR, respectively. : Data presented a linear decrease in mRNA expression of OPN and HOXA10 ( = 0.0066, R = 0.3018 and = 0.0036, R = 0.529, respectively) with women's increasing age, and a similar trend was evident at the protein level (OPN, < 0.05; HOXA10, < 0.01). Further analysis of the data included separating the samples into three age groups: 25-35 years, 36-40 years, and 41-46 years. ANOVA revealed a significant decrease in OPN and HOXA10 mRNA expression ( = 0.03158 and = 0.02578, respectively). CD44 expression did not differ with age. : OPN and HOXA10 are negatively correlated with increasing maternal age. These findings suggest that age-related alterations in key endometrial receptivity modulators may contribute to impaired implantation and could represent potential targets for diagnostic or therapeutic strategies in human implantation failure. - Source: PubMed
Publication date: 2026/04/29
Makrygiannakis FanouriosMarmara MariaVrekoussis ThomasNikitovic DraganaMakrigiannakis AntoniosBerdiaki Aikaterini - The greatest cause of death from breast cancer is metastasis, yet little is known about the molecular mechanisms behind this phenomenon. Using four publically accessible datasets, we conducted a thorough transcriptome analysis of 187 samples from seven breast cancer metastatic sites: the brain, bone, lung, liver, lymph nodes, skin, and local-regional skin (skinlr). Of the 12,005 genes that were found to be shared by all samples in this investigation, 604-885 differentially expressed genes (DEGs) were unique to each metastatic location. Pathways including PI3K-Akt signaling, prolactin signaling, complement, and coagulation cascades were identified by functional enrichment analysis as important metastasis drivers with unique functions in different locales. The results of regulatory analysis revealed 77 upstream factors, including 14 kinases (like EPHB3, PAK3) and 63 transcription factors (like ESR1, FOXA1, and GATA3), some of which were discovered for the first time in breast cancer metastases (like TCF4, HOXA10). It was shown that hub genes including MMP9, SPP1, and PDGFRB are essential for the survival and development of metastases, offering new information on site-specific biology. Crucially, by identifying site-specific molecular markers, these discoveries pave the way for personalized medicine techniques and allow tumor-specific therapy tactics, such as targeting Central Carbon Metabolism in lung and skin metastases. This work provides actionable options for tumor-specific treatment and tailored interventions by highlighting new molecular candidates and signaling pathways for metastatic breast cancer. - Source: PubMed
Publication date: 2026/05/12
Salari AliMikaeili Namini ArshamAlipour AramFarahani FatemehSalehi FarnazShafiei Tehrani Zahra SadatBagherpour GhasemYosefy FatemehJafari DelaramShahbazi AliMirzaei Chegeni MasoumehKhodadad Hossyni Mohammad AminSafari Kharkheshi MahboubehBakhshi Manjili Monire - Homeobox (HOX) genes are essential regulators of embryonic development and cellular differentiation under physiological conditions. Among this gene family, HOXA10 has emerged as a pivotal factor in gastrointestinal (GI) cancers, influencing tumor growth, metastasis, disease progression, and resistance to therapy. HOXA10 functions as a transcription factor and plays key roles not only in embryogenesis but also in immunomodulation. HOXA10 and its transcriptional targets play a crucial role in cancer development, promoting cell growth, invasion, migration, metastasis, and resistance to cell death. Recent studies have explored the influence of HOXA10 on the tumor immune microenvironment, particularly its role in modulating immune cell recruitment and signaling pathways that enable tumor immune evasion. Our recent research identified a HOXA10-regulated five-gene signature that distinguishes long-term from short-term survivors of pancreatic cancer, with HOXA10 expression correlating with increased regulatory T cell (T) infiltration. HOXA10 impacts genes and pathways involving macrophages, Tregs, and other immune cells, potentially creating an immunosuppressive niche that promotes metastasis and diminishes the effectiveness of immunotherapies. In this review, we examine the diverse functions of HOXA10 in GI cancers, offering a comprehensive comparison with other HOX family proteins to elucidate their overlapping and distinct roles in malignancy. Our goal is to provide a thorough overview of how HOXA10 contributes to tumor development and its microenvironment. We highlight its critical role in facilitating cancer progression and metastasis, supported by data from cell lines, patient tumor samples, and clinical studies. Recognizing existing gaps in the understanding of HOXA10's role in cancer, we also explore potential strategies to target this gene, with an emphasis on synergistic approaches that combine HOXA10 inhibition and immunotherapy. Ultimately, these insights aim to identify vulnerabilities within GI cancers that could be exploited through novel therapeutic agents and combination treatments, paving the way for improved clinical outcomes. - Source: PubMed
Publication date: 2026/05/08
Kisling Sophia GShah AshuJohnson EstherAlsafwani Zahraa WRaman VenuBatra Surinder K - MLL-rearranged acute myeloid leukemia (AML) is a high-risk hematological malignancy driven by aberrant epigenetic regulation. MLL fusion proteins recruit the DOT1L methyltransferase, causing dysregulated histone H3K79 methylation and sustained leukemogenic gene expression (HOXA10, MLLT10), while BCL-2 overexpression contributes to apoptosis resistance. This study evaluated the synergistic efficacy of combining the DOT1L inhibitor EPZ004777 with the BCL-2 inhibitor ABT-737. THP-1 cells were treated with EPZ004777 and ABT-737 alone or in combination. Cell proliferation, apoptosis, H3K79 methylation, target gene expression, and PI3K/AKT signaling were assessed. An in vivo xenograft mouse model (C-NKG mice) validated therapeutic effects. Combined treatment exhibited potent synergistic cytotoxicity. Dual inhibition reduced H3K79 di- and tri-methylation, downregulated HOXA10 and MLLT10, and blocked PI3K/AKT phosphorylation. In vivo, combination therapy prolonged survival, restored bone marrow function, and alleviated organ infiltration. These findings demonstrate that dual targeting of DOT1L and BCL-2 exerts synergistic anti-leukemic activity via PI3K/AKT suppression in MLL-rearranged AML, providing a pharmacological rationale for this innovative combination strategy. - Source: PubMed
Publication date: 2026/05/04
Zuo YabeiGeng LiGuo YujieZhao DaitianchangQi NannanWang YanZhang JingyuNiu Zhiyun