PubMed · 5281190
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J Eisinger, B Feuer, T Yamane. 1971-05-26. Codon-anticodon binding in tRNAphe.. https://doi.org/10.1038/newbio231126a0
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Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of effective therapeutic targets to prevent breast cancer metastasis is urgently needed. The function of miR-503-3p has been investigated in other cancers, but its role in breast cancer remains undefined. Here, we found that miR-503-3p was overexpressed in breast cancer tissue and plasma compared with adjacent normal breast tissue and with plasma from healthy individuals. Moreover, we identified miR-503-3p to be an oncogene of breast cancer cell proliferation, migration and invasion. Upregulation of miR-503-3p in breast cancer cells inhibited expression of epithelial-mesenchymal transition (EMT)-related protein SMAD2 and the epithelial marker protein E-cadherin by directly binding to their mRNA 3' untranslated region, whereas increased expression of mesenchymal marker proteins, including vimentin and N-cadherin. Taken together, our findings support a critical role for miR-503-3p in induction of breast cancer EMT and suggest that plasma miR-503-3p may be a useful diagnostic biomarker for breast cancer.
In an earlier study designed to investigate molecular mechanisms of carcinogenesis in synovial sarcomas (SSs), we applied a cDNA microarray to detect human genes with significantly increased expression in SS cells. Among the genes selected in this way, we identified a novel transcript, subsequently designated PDZK4 (PDZ domain-containing 4), that was specifically upregulated in all of the 13 SS cases we examined. On Northern blots of normal human tissues, the PDZK4 transcript was expressed only in fetal brain. Immunocytochemical staining of transfected COS7 cells showed that the PDZK4 gene product localized mainly under the plasma membrane. Treatment of human SS cells with small interfering RNA (siRNA) inhibited the expression of PDZK4 and resulted in the suppression of tumor-cell growth. Induction of exogenous PDZK4 expression promoted growth of T98G and COS7 cells in which no endogenous expression of PDZK4 was observed. Taken together, these findings strongly suggest that inappropriate expression of PDZK4 might play an important role in the proliferation of SS cells and that the gene might be a suitable molecular target for designing of novel drugs to treat SS patients.
1alpha,25-dihydroxyvitamin D3 (vitamin D3) has been shown to upregulate p27Kip1 expression via Sp1 and NF-Y binding sites in the p27Kip1 promoter. However, whether vitamin D3 receptor (VDR) involves in this process is unclear. In this study, we demonstrated that expression of VDR in SW620 cells, which exhibited low level of endogenous VDR, increased vitamin D3-stimulated p27Kip1 promoter activity. On the contrary, suppression of Sp1 expression by small interference RNA reduced the stimulation of p27Kip1 promoter activity by vitamin D3 in LNCaP cells. DNA affinity precipitation assay and chromatin immunoprecipitation assay showed that VDR bound to the p27Kip1 promoter in vitro and in vivo. In addition, we also demonstrated that VDR interacted with Sp1 in vitro and in cells. Collectively, our results suggest that VDR is involved in the induction of p27Kip1 by vitamin D3 and may interact with Sp1 to modulate the expression of target genes that lack VDR response element (VDRE) in their promoters.