Transcriptional regulation of glucose transporters in human oral squamous cell carcinoma cells.
Transcriptional regulation of glucose transporters in human oral squamous cell carcinoma cells.
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DOI：
10.1111/jop.13342
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发表时间：
2022-09
影响因子：
3.3
通讯作者：
Celentano, Antonio
中科院分区：
文献类型：
--
作者：
Paolini, Rita;Moore, Caroline;Matthyssen, Tamara;Cirillo, Nicola;McCullough, Michael;Farah, Camile S.;Botha, Heinrich;Yap, Tami;Celentano, Antonio
在癌细胞中观察到的葡萄糖摄取增加是由葡萄糖转运蛋白（GLUT）介导的，葡萄糖转运蛋白是一类促进葡萄糖和其他底物跨质膜转运的跨膜蛋白。尽管葡萄糖在口腔鳞状细胞癌（OSCC）的病理生理学中起着重要作用，但关于GLUT在口腔粘膜正常或恶性细胞中表达的数据非常有限。我们使用定量聚合酶链反应分析了两种OSCC（H357/H400）和一种非恶性口腔角质形成细胞（OKF 6）细胞系中所有14种GLUT的信使RNA（mRNA）表达。在基线和用两种特异性GLUT抑制剂，即BAY 876（GLUT 1）和WZB 117（GLUT 1、GLUT 3和GLUT 4）治疗后评价GLUT表达。在这里，我们表明，GLUT 1，GLUT 3，GLUT 4，GLUT 5，GLUT 6，GLUT 8，GLUT 12和GLUT 13转录本在所有细胞系中可测量地表达，而GLUT 2，GLUT 7，GLUT 9，GLUT 11和GLUT 14不表达。GLUT 10仅在H357中发现。在BAY 876和WZB 117的存在下，OSCC细胞表现出显着的GLUT的转录谱的改变。特别是，我们观察到GLUT 1，GLUT 3，GLUT 4，GLUT 5和GLUT 6的mRNA响应于选择性GLUT抑制剂的明显增殖依赖性变化。总之，我们首次记录了GLUT 5、GLUT 6和GLUT 12在正常和恶性口腔角质形成细胞中的表达。虽然GLUT转录的调节是细胞系和抑制剂特异性的，但GLUT 3在活跃增殖的OSCC细胞系中持续上调，但在OKF 6中不上调，无论使用何种抑制剂，这表明这种转运蛋白的调节可能是OSCC细胞抑制葡萄糖摄取的主要补偿机制之一。
The increased glucose uptake observed in cancer cells is mediated by glucose transporters (GLUTs), a class of transmembrane proteins that facilitate the transport of glucose and other substrates across the plasma membrane. Despite the important role of glucose in the pathophysiology of oral squamous cell carcinoma (OSCC), there is very limited data regarding the expression of GLUTs in normal or malignant cells from the oral mucosa. We analysed the messenger RNA (mRNA) expression of all 14 GLUTs in two OSCC (H357/H400) and one non‐malignant oral keratinocyte (OKF6) cell line using a quantitative polymerase chain reaction. GLUT expression was evaluated at baseline and after treatment with two specific GLUT inhibitors, namely, BAY876 (GLUT1) and WZB117 (GLUT1, GLUT3 and GLUT4). Here, we show that GLUT1, GLUT3, GLUT4, GLUT5, GLUT6, GLUT8, GLUT12 and GLUT13 transcripts were measurably expressed in all cell lines while GLUT2, GLUT7, GLUT9, GLUT11 and GLUT14 were not expressed. GLUT10 was only found in H357. In the presence of BAY876 and WZB117, OSCC cells exhibited significant alterations in the transcriptional profile of GLUTs. In particular, we observed distinct proliferation‐dependent changes of mRNAs to GLUT1, GLUT3, GLUT4, GLUT5 and GLUT6 in response to selective GLUT inhibitors. In summary, we documented for the first time the expression of GLUT5, GLUT6 and GLUT12 in normal and malignant oral keratinocytes. Whilst regulation of GLUT transcripts was cell line and inhibitor specific, GLUT3 was consistently upregulated in actively proliferating OSCC cell lines, but not in OKF6, regardless of the inhibitor used, suggesting that modulation of this transporter may act as one of the primary compensation mechanisms for OSCC cells upon inhibition of glucose uptake.
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影响因子：
8.5
作者：
Gos, M;Miloszewska, J;Janik, P
通讯作者：
Janik, P
影响因子：
4.8
作者：
Kunkel, Martin;Moergel, Maximilian;Whiteside, Theresa L.
通讯作者：
Whiteside, Theresa L.
影响因子：
5.6
作者：
Celentano, Antonio;McCullough, Michael;Cirillo, Nicola
通讯作者：
Cirillo, Nicola
影响因子：
5.5
作者：
Botha H;Farah CS;Koo K;Cirillo N;McCullough M;Paolini R;Celentano A
通讯作者：
Celentano A
影响因子：
10.6
作者：
Hediger, Matthias A.;Clemencon, Benjamin;Burrier, Robert E.;Bruford, Elspeth A.
通讯作者：
Bruford, Elspeth A.