Ask about this productRelated genes to: SIX1 antibody
- Gene:
- SIX1 NIH gene
- Name:
- SIX homeobox 1
- Previous symbol:
- DFNA23
- Synonyms:
- -
- Chromosome:
- 14q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-29
- Date modifiied:
- 2015-09-02
Related products to: SIX1 antibody
Related articles to: SIX1 antibody
- This study aimed to investigate the role of the homeobox gene SIX1 (sine oculis homeobox homolog 1) in acute myeloid leukemia (AML) progression and to explore its underlying metabolic and immunological mechanisms. SIX1 expression was examined in human bone marrow stromal cells (HS-5) and AML cell lines (HL-60, SKM-1, THP-1, KG-1, NB4, and MOLM13) using RT-qPCR. SIX1-knockdown and SIX1-overexpressing MOLM13 cells were generated by RNA interference and plasmid transfection, respectively. Cell cycle distribution, proliferation, and metabolic parameters, including intracellular glucose, lactate, and ATP levels, were assessed using flow cytometry, EdU incorporation, MTT assays, and ELISA. Mitochondrial content was analyzed by transmission electron microscopy. Peripheral blood mononuclear cells (PBMCs) from healthy donors were co-cultured with genetically modified MOLM13 cells under low-glucose conditions to evaluate T-cell proportions and cytokine production (IL-6, TNF-α, and IFN-γ). An AML mouse model was further established to assess the effects of SIX1 on T-cell composition and function by flow cytometry, while global metabolomics was applied to characterize metabolic reprogramming in vivo. SIX1 was significantly up-regulated in AML cells and promoted MOLM13 cell proliferation by enhancing glycolytic metabolism. Moreover, SIX1 suppressed CD8⁺ T-cell effector function both in vitro and in vivo and was associated with extensive alterations in amino acid, glucose, and lipid metabolism in AML mice. SIX1 facilitates AML progression by promoting glycolytic reprogramming in leukemia cells and potentially impairing CD8⁺ T-cell effector function through metabolic competition, highlighting SIX1 as a promising therapeutic target. - Source: PubMed
Publication date: 2026/09/04
Hou HuiLi RuijunZhao LeiMa YanZhao JingjingLi JunliLiu JianpingWang YuminZhang Luqiang - Wilms tumor (nephroblastoma) is a pediatric renal malignancy driven by disrupted nephrogenesis, yet its transcriptomic relationship with ferroptosis and immune remodeling remains poorly characterized. - Source: PubMed
Publication date: 2026/08/17
Li GuijunBai JinhongHu SaiGao XiuliWang FangLi Song - : As a member of the T-box transcription factor family, TBX18 was found to be involved in ESCC progression, while its role in regulating radiotherapy resistance in ESCC remains unclear. This study was designed to investigate the molecular mechanisms underlying the regulation of radioresistance in ESCC by TBX18. : Sphere formation assay, Transwell invasion assay, and wound healing assay were conducted to show the influence of TBX18 on tumor stemness and epithelial-mesenchymal transition (EMT). Western blot, immunofluorescence, chromatin immunoprecipitation-qPCR (ChIP-qPCR) and dual-luciferase reporter assay were preformed to identify regulatory networks. A nude mouse xenograft tumor model was established to assess the regulatory effect of TBX18 and SIX1 on radioresistance of ESCC in vivo. : TBX18 expression was positively associated with stemness markers, including CD44, CD271, and SOX2. TBX18 promoted stemness-associated phenotypes, EMT, migration, invasion, and radioresistance in ESCC cells. Mechanistically, TBX18 directly bound to the SIX1 promoter and transcriptionally activated SIX1 expression. In turn, SIX1 enhanced TBX18 protein stability by suppressing ubiquitin-proteasome-mediated degradation, thereby forming a positive feedback loop. Functional rescue experiments demonstrated that the TBX18/SIX1 axis coordinately maintained stemness and EMT phenotypes and attenuated radiotherapy-induced apoptosis. In vivo studies further confirmed that TBX18 knockdown enhanced radiosensitivity, whereas SIX1 overexpression partially reversed this effect. In addition, immunohistochemical analysis revealed that TBX18 and SIX1 were significantly upregulated in ESCC tissues and positively correlated with each other. - Source: PubMed
Publication date: 2026/08/20
Gu LimingYang TianqiZhang JinmengWu JiaFan QiangZhang YunxiaChe JunZhu JunGu KeZhou Jialiang - The anterior pituitary integrates endocrine regulation, cellular growth, and adaptive responses. Adipokines, secreted mainly by adipose tissue, act as hormonal signals linking metabolism, inflammation, appetite, and reproduction. They regulate hypothalamic-pituitary-ovarian axis by modulating hormone secretion and intracellular signaling. The presence of adipokine receptors in anterior pituitary suggests local metabolic-endocrine interactions. Omentin-1, predominantly expressed in visceral adipose tissue, participates in glucose metabolism and ovarian steroid regulation. Recent findings indicate that omentin-1 modulates tropic hormones, their receptors, and adipokine balance in anterior pituitary cells. We hypothesized that omentin-1 affects protein expression and signaling pathways involved in pituitary cell proliferation and apoptosis. This study examined its effects in anterior pituitary cells from Large White and Meishan pigs. Proteomic analysis identified 230 candidate differentially abundant proteins after omentin-1 treatment: 30 downregulated and 3 upregulated in Large White pigs, and 107 downregulated and 90 upregulated in Meishan pigs, associated with enriched 116 Gene Ontology terms. Key proteins were associated with cell cycle, DNA replication, gene expression, and posttranscriptional/posttranslational regulation. Responses differed between breeds. CDK5RAP2 and SIX1 were linked to proliferative control in Large White pigs, whereas AKT1S1 and RHOA were among the proteins associated with the broader proteomic response observed in Meishan pigs. Meishan pigs showed dynamic apoptotic protein regulation, including HTRA2, PARP2, and DFFA. Complementary in vitro experiments demonstrated that omentin-1 downregulated cyclins and caspase-3, upregulated BCL2, increased BCL2/BAX ratio, and modulated ERK1/2, AKT, AMPKα, and STAT3 phosphorylation. Together, these findings suggest that omentin-1 modulates proteomic networks and intracellular signaling associated with anterior pituitary cell function during the mid-luteal phase of the estrous cycle. - Source: PubMed
Publication date: 2026/08/19
Respekta-Długosz NataliaKubicka KarolinaGreggio AleksandraŚwiderska BiankaMalinowska AgataRytelewska EdytaOpydo MałgorzataDupont JoëlleKamiński TadeuszSmolińska NinaRak Agnieszka - Lactylation, a lactate-dependent posttranslational modification, is involved in cancer development. Here, we showed that GCN5L2 physically interacts with nuclear SIX1 and acts as a key regulator of SIX1 lactylation. GCN5L2 depletion promotes APC/Cdh1 binding to SIX1, increases SIX1 ubiquitination, and reduces SIX1 protein stability. Functionally, the GCN5L2-SIX1 axis promotes glucose uptake, glycolysis process, and energy supply in TNBC cells. GCN5L2 knockdown attenuates the growth and migration of TNBC cells, and increases the sensitivity of TNBC cells to paclitaxel. Overexpression of SIX1 reverses the GCN5L2 knockdown-induced glycolysis and growth suppression in TNBC cells. In addition, GCN5L2 expression is enriched and positively correlated with SIX1 in clinical TNBC tissues. More importantly, we demonstrated 9‴-Methyl salvianolate B as a candidate modulator of the GCN5L2-SIX1 complex via an unbiased screening. 9‴-Methyl salvianolate B suppresses the GCN5L2-SIX1 axis and blocks the glycolysis, proliferation, metastasis, and paclitaxel resistance of TNBC cells. Overall, this study highlights the significance of the GCN5L2-SIX1 axis in sustaining glycolysis and TNBC development, and provides experimental evidence of 9‴-Methyl salvianolate B as a candidate modulator of the GCN5L2-SIX1 axis, presenting a promising strategy for TNBC management. - Source: PubMed
Publication date: 2026/08/14
Liao YuningYin ShushaPeng E-YingWu JinjieYao YuHe WanyingHuang HongbiaoLiu QingDeng YuanfeiYao LeyiCai Gengxi