Ask about this productRelated genes to: DLX4 antibody
- Gene:
- DLX4 NIH gene
- Name:
- distal-less homeobox 4
- Previous symbol:
- DLX7, DLX9
- Synonyms:
- DLX8, BP1
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-07
- Date modifiied:
- 2016-10-25
Related products to: DLX4 antibody
Related articles to: DLX4 antibody
- Cutaneous melanoma, a highly aggressive and therapy-resistant skin cancer, is characterized by its remarkable cellular plasticity, enabling tumour cells to switch between different phenotypic states. This plasticity contributes to tumour heterogeneity and is regulated by key transcription factors. Long non-coding RNAs (lncRNAs) are emerging as crucial regulators in melanoma progression, yet much remains to be explored regarding their role in phenotype switching. In this study, we analysed long non-coding RNAs (lncRNAs) across different murine melanoma cell lines, identifying a set of lncRNAs potentially involved in regulating melanoma phenotypic state through cis-regulation of neighbouring protein-coding genes. We demonstrated that the lncRNA regulates genes associated with melanoma plasticity, favouring a mesenchymal-like, undifferentiated state. knockdown redirected melanoma cells to a more differentiated and less malignant phenotype, confirmed by differential expression of phenotypic state markers (), reduced their invasive and migratory potential, and delayed tumour progression . Furthermore, we identified a human orthologue of . Our findings highlight the potential of as both a biomarker and therapeutic target, capable of modulating melanoma's phenotypic plasticity to influence treatment response and metastasis. - Source: PubMed
Publication date: 2026/03/19
Ayub Ana Luisa PedrosoTonin Beatriz Cristina BizAzevedo HátylasJordão Pedro Henrique FogaçaSaxena TanviSejour LeinalNsengimana JeremieVlachos IoannisReis Eduardo MoraesSlack Frank JohnJasiulionis Miriam Galvonas - Distal - less homeobox 4 (DLX4) is a transcription factor vital for embryonic development and shows pro - oncogenic properties in some hematological and solid tumors. In colorectal cancer (CRC), its molecular function and contributions to tumorigenesis remain to be explored. Using bulk, single - cell and spatial transcriptomics, we assessed DLX4’s clinicopathological significance and its impact on the tumor immune microenvironment (TIME). Our results show DLX4 is highly expressed in CRC, correlating with poor prognosis in multi - center cohorts and is also related to a cytotoxic T lymphocyte (CTL) dysfunction - related immunosuppressive microenvironment. Transcriptomic and proteomic analyses identified DLX4 - associated cell signaling. In vitro, we confirmed DLX4 promotes cell proliferation, cell - cycle transitions and suppresses apoptosis. Furthermore, we found its key transcriptional target ZC3HC1 via ChIP – seq analysis, ChIP - qPCR and luciferase assay. Notably, DLX4 has strong potential for liquid - liquid phase separation and likely forms condensates when binding to ZC3HC1’s promoter, a crucial cell - cycle regulator. Overall, DLX4 is a novel prognostic biomarker and suggests potential CRC therapeutic strategies, making significant contributions to the understanding and potential treatment of CRC at the molecular level. - Source: PubMed
Publication date: 2025/10/22
Cheng JingsongZhang ChengxiLuo YimanChen YihanChen NantingWan YuanyuanHuang XinyuZheng ZihengYin QingyaoChen XueHua JingLi YangHuang Rongzhong - The fibroblast-like synoviocyte (FLS) has a central role in rheumatoid arthritis (RA) pathogenesis and its invasive behavior strongly correlates with disease severity and joint damage. Yet, the regulation of FLS invasiveness is incompletely understood. Distal-less homeobox 4 (DLX4) is a transcription factor implicated in cancer cell invasion and metastasis, and we considered that it might also be involved in the regulation of FLS phenotypes. siRNA was used to knockdown DLX4 in RA FLS, compared with a control siRNA. Cells were then studied in invasion, migration, proliferation and adhesion assays, and RNA was used for RNA sequencing and pathway analyses. siRNA knockdown of DLX4 significantly reduced RA FLS invasiveness (P = 0.028) and migration in the scratch/wound healing assay (P = 0.008). RNA sequencing analyses revealed that DLX4 knockdown significantly affected processes and pathways implicated genes involved in diverse types of cancer and in cancer biology, including cell invasion, cell cycle, DNA replication, transcription, p53 signal transduction, RHO GTPase signaling, regulation of cytokinesis, as well as response to oxygen levels and to oxidative stress. HMOX1 and SOD2 were among the genes with the most significantly increased expression, while CPNE3 and HADHA were among those with the most significantly decreased expression in FLS knocked down for DLX4 compared with controls. We describe a new role for DLX4 in the regulation of RA FLS behaviors relevant to disease pathogenesis and joint damage, and identify a new transcriptomic signature regulated by this gene. These findings raise the possibility that DLX4, or one of its target genes and pathways may become a target for treatment. - Source: PubMed
Publication date: 2025/07/11
Laragione TeresinaHarris CarolynGulko Percio S - DLX4 is involved in the regulation of embryonic development, but its function in cancer remains unclear. Here, we conducted a pan-cancer analysis to investigate the molecular mechanisms of DLX4, with a particular emphasis on its role in renal cancer. - Source: PubMed
Publication date: 2025/04/05
Kou ZengshunZhu ShuaizhiZhu JiaxiWang ShufeiZheng YuZhou ShengjieSi Zi'angZhu Hai - Short-term and long-term adverse events could occur after general anesthesia (GA) and the specific mechanism driving these effects has not yet been well-characterized. In this study, we aimed to evaluate the global effect of GA on DNA methylation in the cell-free DNA (cfDNA) of surgical lung-nodule patients. - Source: PubMed
Publication date: 2024/11/13
Liang WenhuaLiu XinChen ZhuxingWang HaixuanYu ZiwenLi ChunyanYang HaoTao JinshengLi HuiChen ZhiweiFan Jian-BingHe Jianxing