The present study provides a detailed comparative description in the adult rat brain of areas that express mRNAs coding for the fibroblast growth factor subtype receptors 1-3 (FGFR1-3). One observation in this analysis was a widespread expression in the brain of all three FGFR mRNAs, according to the following rank order: FGFR1, diencephalon < telencephalon < mesencephalon and metencephalon < myelencephalon; FGFR2 and FGFR3, telencephalon < diencephalon < mesencephalon and metencephalon < myelencephalon. Another observation was an apparent cellular specificity in their basal expression. Thus, the FGFR1 mRNA was expressed mainly in large and weakly stained cells, whereas FGFR2 transcripts were expressed primarily in small and strongly stained cells and in cells of brain regions devoid of neuronal cells, such as the white matter. FGFR3 mRNA was always detected in small and strongly stained cells with scattered distribution and was not expressed in the white matter. However, FGFR2 mRNA was weakly expressed also in large cells localized in some nuclei of the lower brainstem, in the diagonal band, and in the septum. Furthermore, in the medial habenula and in the nuclei of the pons, there exists a high density of cells expressing both FGFR1 and FGFR2 (60-100%). With neurotoxic lesions involving 6-hydroxydopamine microinjections in the substantia nigra, reactive glial cells in the lesioned area and surrounding the cannula tract showed an increase in the expression of both FGFR1 and FGFR2 mRNAs, whereas no increased expression was found for FGFR3 mRNA. Taken together, these findings showed that these three FGF receptors exist in all subtypes of cells of each brain region. Their apparent cellular specificity suggests that these receptor subtypes can have a differential trophic role in the brain, reflecting the various biological activities shown by the ligands of the FGF family.

Increasing evidence indicated that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) acted as a key regulator in the proliferation and invasion of several cancers. However, the function of MALAT1 in the development of cholangiocarcinoma has not been experimentally established. In the present study, the expression levels of MALAT1 in cholangiocarcinoma cell lines were detected by quantitative real-time PCR. The effects of MALAT1 knockdown on the cell proliferation and invasion of cholangiocarcinoma cells were detected with Cell Counting Kit-8 (CCK-8), colony formation assay and Trans-well assay, respectively. The expressions of epithelial-mesenchymal transition (EMT)-related proteins (E-cadherin, Vimentin) were evaluated to discover whether the process of EMT was involved. We also evaluated the expression of phos-phatidylinositol-3-kinase/serine/threonine kinase (PI3K/Akt) signaling pathway proteins (PI3K, p-PI3K, Akt, p-Akt) to determine the associated molecular mechanism. And we discovered that MALAT1 was up-regulated in cholangiocarcinoma cancer cells. CCK-8, colony formation and trans-well assay showed that the proliferation and invasion of QBC-939 and RBE with MALAT1 knockdown were inhibited. Moreover, MALAT1 could promote EMT in cholangiocarcinoma cells. In addition, MALAT1 may activate PI3K/Akt pathway. These results indicated that MALAT1 promoted cholangiocarcinoma cell proliferation and invasion. The effects of MALAT1 on cholangiocarcinoma cells might be through activating the PI3K/Akt signaling pathway. These investigations may facilitate a better understanding of MALAT1 and it might be a potential therapeutic target for the treatment of cholangiocarcinoma.

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