PurposeMicroRNAs (miRNAs) are a major class of small endogenous RNA molecules that posttranscriptionally regulate the expression of most genes in the human genome. miRNAs are often located in chromosomal fragile sites, which are suscept-ible to amplification or deletion. Chromosomal deletions are frequent events in breast cancer cells. Deletion and loss of heterozygosity at 17p13.3 have been reported in 49% of breast cancers. The aim of the current study was to evaluate potential expression alterations of miR-22, miR-132, and miR-212, which are located on the 17p13.3 locus and are required for mammary gland development.MethodsA matched case-control study was conducted, which included 36 pairs of tumor and matched nontumor surgical specimens from patients diagnosed with breast invasive ductal carcinoma. Formalin-fixed paraffin-embedded samples from archival collections at the pathology department of Shariati Hospital were prepared for RNA extraction using the xylene-ethanol method before total RNA was isolated with TRIzol Reagent. Specific primers were designed for cDNA synthesis and miRNA amplification. The expression of miRNAs was then evaluated by real-time polymerase chain reaction (RT-PCR).Results According to our RT-PCR data, the miR-212/miR-132 family was downregulated in breast cancer (0.328-fold, p<0.001), and this reduced expression was the most prominent in high-grade tumors. In contrast, miR-22 exhibited a significant upregulation in breast tumor samples (2.183-fold, p=0.040).ConclusionConsistent with the frequent deletion of the 17p13.3 locus in breast tumor cells, our gene expression data demonstrated a significant downregulation of miR-212 and miR-132 in breast cancer tissues. In contrast, we observed a significant upregulation of miR-22 in breast tumor samples. The latter conflicting result may have been due to the upregulation of miR-22 in stromal/cancer-associated fibroblasts, rather than in the tumor cells.
Purpose: Lung cancer is responsible for more cancer-related death worldwide Most lung cancer patients have non-small cell lung cancers (NSCLC), with low survival rate. Therefore, it is necessary to study new and effective targeted therapies. Discoidin domain receptor1 (DDR1) is a tyrosine kinase receptor that reacts to various collagens. Expression of DDR1 can be promoted by collagen type I, and dysregulation of DDR1 signaling are involved in several phases of tumorigenesis. Tumor growth and metastasis depend on angiogenesis caused by angiogenic factors, such as vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) secreted by tumor cells. Thus, Angiogenesis plays a critical role in cancer progression and inhibition of angiogenesis is essential for cancer treatment. The aim of the current study was to evaluate the alteration of DDR1 expression and its effects on VEGF-A, FGF-1, and FGF2 in NSCLC.Methods: A549 and Calu-3 cell lines, were treated with collagen type I and transfected with DDR1 small interfering RNA (siRNA). Then, the relative expression of DDR1, VEGF-A, FGF-1, and FGF-2 was evaluated using quantitative real-time polymerase chain reaction (qRT-PCR). The concentration of angiogenic factors was calculated by Human Angiogenesis 17-plex discovery assay. Results: According to our data, the collagen type I could stimulate DDR1 expression and DDR1 upregulation resulted in a significant increase of VEGF-A and FGF-2 expression, but did not induce FGF-1 expression. Moreover, DDR1 downregulation significantly decreased VEGF-A and FGF-2 expression. Conclusion: our findings suggest that alteration of DDR1 expression may affect VEGF-A and FGF-2 expression in NSCLC associated with tumor angiogenesis and represent a new treatment approach.
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