There are still not specified mechanisms how beta-glucan molecules are transported into cells. Supposing, beta-glucan toxicity against tumor cells may be related to the overexpression of the transporter responsible for the transport of glucose molecules in the cells. In this case, glucans - polymers composed of glucose units are much more up-taken by tumor than normal cells. Increased GLUT1 (Glucose Transporter Type 1) expression has been demonstrated earlier in malignant melanomas. GLUT1 expression promotes glucose uptake and cell growth in that cells. Also, in human melanoma tissues a significant correlation between GLUT1 expression and mitotic activity was found.

The aim of the study was to verify if oat β-glucan (OβG) is delivered into cells by GLUT-1 membrane protein. To check it out we blocked GLUT1 transporters by an inhibitor WZB117 and then we investigated cells viability with and without reversible electroporation (EP).

The obtained results bring us to elucidate the mechanism of transport of the OβG into the cells is GLUT-1 dependent and moreover can be supported by EP method.

β-葡聚糖分子如何被转运到细胞中，仍然没有明确的机制。假设β-葡聚糖对肿瘤细胞的毒性可能与负责葡萄糖分子在细胞中转运的转运蛋白的过表达有关。在这种情况下，葡聚糖-由葡萄糖单元组成的聚合物比正常细胞更容易被肿瘤吸收。GLUT1（1型葡萄糖转运蛋白）表达增加已在恶性黑色素瘤中得到证实。GLUT1表达促进该细胞中葡萄糖的摄取和细胞生长。同样，在人黑素瘤组织中，发现GLUT1表达与有丝分裂活性之间存在显着相关性。

该研究的目的是验证燕麦β-葡聚糖（OβG）是否通过GLUT-1膜蛋白传递到细胞中。为了证实这一点，我们用抑制剂WZB117阻断了GLUT1转运蛋白，然后研究了有无可逆电穿孔（EP）的细胞活力。

所获得的结果使我们阐明了OβG向细胞内转运的机制是GLUT-1依赖性的，而且可以通过EP方法得到支持。