目的 检测微小RNA（miR）在人黑色素瘤中的表达情况,研究miR-412通过抑制性别确定区Y框转录因子6（SOX6）的表达影响黑色素瘤细胞增殖及侵袭能力的变化。方法 癌症基因组图谱（TCGA）数据库分析发现miR-412在黑色素瘤中异常表达,为研究其表达与肿瘤的相关性,采用Transwell小室,非锚定独立生长实验分析miR-412对黑色素瘤细胞增殖及侵袭能力的影响。软件预测SOX6可能为其靶向基因,采用荧光素酶报告分析及Western blot实验检测SOX6与miR-412的靶向调节情况。结果 TCGA数据库分析黑色素瘤组织中miR-412表达水平高于正常对照组,表达越高,生存时间越短。Transwell小室,非锚定独立生长实验显示miR-412过表达后促进细胞增殖及侵袭能力,而下调miR-412后抑制黑色素瘤细胞增殖及侵袭能力;通过靶点预测miR-412结合SOX6基因3’-非翻译区（UTR）,导致SOX6蛋白因miR-412表达增高而下调;同时在miR-412下调的细胞中抑制SOX6表达可恢复黑色素瘤细胞的增殖及侵袭能力。结论 miR-412过表达后促进黑色素瘤细胞增殖及侵袭能力,反之则抑制黑色素瘤细胞增殖及侵袭能力。 miR-412通过靶向调控SOX6影响黑色素瘤细胞增殖及侵袭,提示miR-412在黑色素瘤的发病过程中起重要作用,是潜在的治疗靶点。

Objective To assess the expression of miR-412 in human melanoma and investigate how miR-412 modulates melanoma cell proliferation and invasive capacity by inhibiting SRY-Box Transcription Factor 6,（SOX6） expression．Methods Analysis of the TCGA（The Cancer Genome Atlas）database identified aberrant miR-412 expression in melanoma．To explore its relevance to tumorigenesis,we conducted Transwell chamber and non-adherent independent growth assays to examine the effects of miR-412 on melanoma cell proliferation and invasion．Software predictions highlighted SOX6 as a potential target gene．We performed luciferase reporter assays and Western blot experiments to elucidate the regulatory interactions between SOX6 and miR-412．Results TCGA database analysis revealed significantly elevated miR-412 expression levels in melanoma tissues compared to the normal control group．Moreover,higher miR-412 expression correlated with shorter survival times．Functional assays using Transwell chambers and non-adherent independent growth assays demonstrated that overexpressing miR-412 enhanced cell proliferation and invasive capabilities．Conversely,reducing miR-412 expression restrained these attributes in melanoma cells． Target prediction analysis indicated that miR-412 binds to the 3’-UTR region of SOX6,resulting in decreased SOX6 protein levels due to increased miR-412 expression．Intriguingly,inhibiting SOX6 expression concurrently amplified the proliferation and invasive potential of melanoma cells,which was initially dampened by miR-412 downregulation．Conclusions Elevated miR-412 expression augments melanoma cell proliferation and invasive capabilities,while its suppression diminishes these traits．Through its targeted regulation of SOX6,miR-412 exerts a significant influence on melanoma cell proliferation and invasion．These findings underscore the pivotal role of miR-412 in melanoma pathogenesis and underscore its potential as a promising therapeutic target．

目的 氧化苦参碱对视网膜母细胞瘤细胞SM-106凋亡的诱导作用及机制。方法 以不同作用时间(24 h、48 h、72 h)和不同作用浓度(12.5 μl/mL、25 μl/mL、50 μl/mL、100 μl/mL)氧化苦参碱处理视网膜母细胞瘤细胞SM-106,分别采用流式细胞仪及western blot检测视网膜母细胞瘤细胞SM-106细胞凋亡及其凋亡因子(Bax、Bcl-2)蛋白表达。结果 氧化苦参碱可促进SM-106细胞体外凋亡,上调Bax蛋白表达及Bax/Bcl-2蛋白表达比值,下调Bcl-2蛋白表达,并呈现剂量及时间依赖性。结论 氧化苦参碱可诱导视网膜母细胞瘤细胞SM-106凋亡,调控凋亡因子Bax、Bcl-2的表达是其可能作用机制。

Objective To evaluate the apoptosis and its mechanism of retinoblastoma cells SM-106 induced by oxymatrine. Methods Retinoblastoma cells SM-106 were treated with different time(24 h、48 h、72 h)and different concentrations(12.5 μl/mL, 25 μl/mL, 50 μl/mL or 100 μl/mL) of oxymatrine. The apoptosis and protein expression of apoptosis factors (Bax and Bcl-2) were respectively determined by flow cytometry and western blot. Results Oxymatrine significantly promoted the SM-106 cells apoptosis in vitro, raised Bax protein expression and Bax/Bcl-2 protein expression ratio, reduced the Bcl-2 protein expression, and showed the dose and time dependent. Conclusion Oxymatrine is able to induce the apoptosis in retinoblastoma cells SM-106. Regulating apoptosis related gene Bax and Bcl-2 expression may be the mechanism of apoptosis.