کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3039777 | 1579683 | 2015 | 6 صفحه PDF | دانلود رایگان |
• Gene and protein levels of ECM molecules in human brain samples were examined.
• Differences in the peritumoral and normal tissues were revealed.
• We could identify molecules that may affect the peritumoral invasion processes.
• ECM of peri-glioblastoma does not react definitely to the spreading of the tumour.
• Peri-metastatic ECM changes can probably decrease tumour infiltration.
ObjectiveThe effectiveness of therapy of intracerebral neoplasms is mainly influenced by the invasive behaviour of the tumour. The peritumoral invasion depends on the interaction between the tumour cells and the extracellular matrix (ECM) of the surrounding brain. The invading tumour cells induce change in the activity of proteases, synthases and expression of ECM-components. These alterations in the peritumoral ECM are in connection to the highly different invasiveness of gliomas and metastatic brain tumours. To understand the fairly modified invasive potential of anaplastic intracerebral tumours of different origin, the effect of tumour on the peritumoral ECM and alterations of invasion related ECM components in the peritumoral brain were evaluated.MethodsFor this reason the mRNA expression of 19 invasion-related molecules by quantitative reverse transcriptase polymerase chain reaction was determined in normal brain tissue (Norm), in the peritumoral brain tissue of glioblastoma (peri-GBM) and of intracerebral adenocarcinoma metastasis (peri-Met). To evaluate the translational expression of the investigated molecules protein levels were determined by targeted proteomic methods.ResultsEstablishing the invasion pattern of the investigated tissue samples 8 molecules showed concordant difference at mRNA and protein levels in the peri-GBM and peri-Met, 11 molecules in the peri-Met and normal brain and 12 in the peri-GBM and normal brain comparison.ConclusionOur results bring some ECM molecules into focus that probably play key role in arresting tumour cell invasion around the metastatic tumour, and also in the lack of impeding tumour cell migration in case of glioblastoma.
Journal: Clinical Neurology and Neurosurgery - Volume 139, December 2015, Pages 138–143