背景:微RNA(miRNA)是公认的翻译后非编码RNA,在mRNA降解和抑制中起关键作用。葡萄糖转运蛋白1(GLUT1)与各种miRNA显示出相关性,特别是miRNA10a在肺癌中的表达。miRNA10a以及葡萄糖上调导致口腔鳞状细胞癌(OSCC)中癌症增殖的作用尚不清楚。本研究旨在探讨miRNA10a和GLUT1在OSCC合并糖尿病患者中的表达水平。
方法:在OSCC中估计miRNA10a和GLUT1的表达,癌前病变,和健康组织使用定量逆转录酶聚合酶链反应(RT-PCR)。将miRNA10a和GLUT1表达水平记录为倍数变化。Further,进行了单向方差分析(ANOVA)检验,以发现OSCC之间miRNA10a和GLUT1表达是否有任何差异,癌前病变,和健康的组织。
结果:RT-PCR结果显示,与癌前组织和健康组织相比,OSCC中miRNA10a和GLUT1的表达增加。在潜在的恶性组织和对照组织中,miRNA10a和GLUT1表达水平之间存在正相关,癌变组织明显增加.这项研究证明了上调miRNA10a表达的意义,表明通过GLUT1过表达与OSCC增殖直接相关。具体来说,miRNA10a在潜在恶性组织中表现出1.2±0.072的倍数变化,在癌组织中表现出1.4±0.05的倍数变化,而GLUT1在潜在恶性组织中表现出1.25±0.092的倍数变化,在癌组织中表现出0.092±0.08的倍数变化,分别。
结论:这项研究强调了miRNA10a在癌组织中通过调节GLUT1促进增殖,从而在癌症进展中的作用。特别是在高血糖情况下。这种机制进一步有助于增加癌症患者的葡萄糖转运,这可能会阻碍肿瘤的预后。这些发现强调了靶向miRNA10a和GLUT1作为癌症治疗干预的潜在意义。
BACKGROUND: MicroRNAs (miRNAs) are well-established post-translational non-coding RNAs that play crucial roles in mRNA degradation and repression. Glucose transporter 1 (GLUT1) showed correlation along with various miRNA, specifically miRNA10a expression in lung cancers. The role of miRNA10a along with glucose upregulation leading to cancer proliferation in oral squamous cell carcinoma (OSCC) is unknown. This study aimed to investigate the expression levels of miRNA10a and GLUT1 in OSCC patients with diabetes.
METHODS: miRNA10a and GLUT1 expression were estimated in OSCC, precancerous, and healthy tissues using quantitative reverse transcriptase polymerase chain reaction (RT-PCR). miRNA10a and GLUT1 expression levels were recorded as fold change. Further, a one-way analysis of variance (ANOVA) test was performed to find whether there is any difference in miRNA10a and GLUT1 expression between OSCC, precancerous, and healthy tissues.
RESULTS: The RT-PCR findings revealed an increased expression of miRNA10a and GLUT1 in OSCC compared to precancerous and healthy tissue. There is a positive correlation between miRNA10a and GLUT1 expression levels in both potentially malignant and control tissues, with a marked increase in cancerous tissue. This study demonstrated the significance of upregulated miRNA10a expression, indicating a direct correlation with OSCC proliferation via GLUT1 overexpression. Specifically, miRNA10a exhibited a fold change of 1.2±0.072 in potentially malignant tissue and 1.4±0.05 in cancer tissue, while GLUT1 exhibited a fold change of 1.25±0.092 in potentially malignant tissue and 0.092±0.08 in cancer tissue, respectively.
CONCLUSIONS: This research highlights the role of miRNA10a in cancer progression by facilitating proliferation through the regulation of GLUT1 in cancerous tissues, particularly in hyperglycemic conditions. This mechanism further contributes to increased glucose transport in cancer patients, which may potentially impede tumor prognosis. These findings underscore the potential significance of targeting miRNA10a and GLUT1 as therapeutic interventions in cancer management.