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There is not enough information about MT gene expression changes in different grade gliomas.
Also, MT gene expression alterations are associated with carcinogenesis and with aggressive tumour behaviour and even chemotherapy resistance11.
It is known that MT gene expression in glioblastoma tumour samples was related to shorter patients survival16.
For instance, MT gene expression was associated with tumour grade and cell proliferation rate in germ cell carcinoma and breast cancer12,15.
For the MT gene expression and methylation analysis in total 55 samples were analysed as follows: I-III malignancy grade astrocytic gliomas (n = 17) and GBM (n = 38).
MT gene expression was normalized to healthy human brain RNA samples (RHB) "Total RNA-Human Adult Normal Tissue 5 donor Pool: Brain" (BioChain) using 2−ΔΔCt method where ΔΔCt = ΔCttumour tissue (CtMT − Ctβ-actin)− ΔCtRHB (CtMT − Ctβ-actin).
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D.S. generated an idea, conception, and design of the study, B.M. designed qPCR primers, B.M. & I.V. performed MTs gene expression analysis.
We further examined the possible alterations of MTs gene expression during the formation of cross-adaptation response to neurobehavioral toxicity induced by metal exposure.
These findings clearly suggested that hsa-miR-mit3 and hsa-miR-mit4 may downregulate MT-RNR2 gene expression and that the 3′ UTR of MT-RNR2 is the possible target for hsa-miR-mit3 or hsa-mir-mit4 microRNA.
MT-3 gene expression was then examined by RT-PCR in preadipocytes.
Data showed that hsa-miR-mit3 and hsa-miR-mit4 downregulate MT-RNR2 gene expression.
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