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mir-199a-5p cooperatively suppress mir-199a-5p metastasis epithelial month download article/chapter mir-199a-5p led mir-199a-5p loss mir-199a-5p resulted bcr-abl p210 transcripts human prostate cancer article digestive diseases real-time rt-pcr mir-199a-5p central south university full article pdf increased e-cadherin expression e-cadherin promotor methylation luciferase reporter assay human colorectal cancer microrna-199a-5p fibroblasts promotes metastasis epithelial-mesenchymal transition colorectal cancer cells privacy choices/manage cookies receptor tyrosine kinases discoidin domain receptors1 related subjects liver metastasis breast cancer cells electronic supplementary material colorectal cell proliferation colorectal cancer development global cancer statistics affiliated cancer hospital post-transcriptional regulation epithelial-mesenchymal transitions ziyuan tang emt-related signaling curr drug targets article hu signaling regulator grp78 promoter methylation contributes clin cancer res extracellular discoidin i breast carcinoma cells european economic area relative signal pathways directly target ddr1 hippo-yap pathway distinct structural characteristics conserved seed pairing endoplasmic reticulum chaperone

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         description:Discoidin domain receptors1 (DDR1) is associated with tumor progression, and its dysregulated expression has been observed in many cancers. We aim to explore molecular mechanism underlying the role of DDR1 in colorectal cancer development. Immunohistochemistry and Western blot were applied to examine the DDR1 expression. Real-time RT-PCR and Western blot were performed to determine the expression of miR-199a-5p and DDR1. Luciferase reporter assay was used to determine whether DDR1 was a target of miR-199a-5p. Effects of miR-199a-5p and DDR1 on colorectal cell proliferation, colony formation, cell cycle progression, invasion and migration were then investigated. Western blot was used to determine the relative signal pathways. Increased DDR1 and decreased miR-199a-5p expression coexisted in CRC, knockdown of DDR1 or overexpression of miR-199a-5p both resulted in reduced colony formation, invasive and migratory capabilities of human CRC LOVE1 and LOVO cells. It was also found that overexpression of miR-199a-5p led to decreased DDR1, MMP2, N-cadherin and vimentin expression and increased E-cadherin expression in both CRC cell lines. However, down-regulation of miR-199a-5p resulted in the opposite effects. Dual luciferase reporter assay confirmed that miR-199a-5p could directly target DDR1 through binding to its 3′-UTR. Our findings indicated that up-regulation of DDR1 induced by miR-199a-5p down-regulation may contribute to the development and progression of CRC, and this effect may be associated with increased invasiveness, at least in part, via activating the EMT-related signaling.
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      headline:MiR-199a-5p Loss Up-Regulated DDR1 Aggravated Colorectal Cancer by Activating Epithelial-to-Mesenchymal Transition Related Signaling
      description:Discoidin domain receptors1 (DDR1) is associated with tumor progression, and its dysregulated expression has been observed in many cancers. We aim to explore molecular mechanism underlying the role of DDR1 in colorectal cancer development. Immunohistochemistry and Western blot were applied to examine the DDR1 expression. Real-time RT-PCR and Western blot were performed to determine the expression of miR-199a-5p and DDR1. Luciferase reporter assay was used to determine whether DDR1 was a target of miR-199a-5p. Effects of miR-199a-5p and DDR1 on colorectal cell proliferation, colony formation, cell cycle progression, invasion and migration were then investigated. Western blot was used to determine the relative signal pathways. Increased DDR1 and decreased miR-199a-5p expression coexisted in CRC, knockdown of DDR1 or overexpression of miR-199a-5p both resulted in reduced colony formation, invasive and migratory capabilities of human CRC LOVE1 and LOVO cells. It was also found that overexpression of miR-199a-5p led to decreased DDR1, MMP2, N-cadherin and vimentin expression and increased E-cadherin expression in both CRC cell lines. However, down-regulation of miR-199a-5p resulted in the opposite effects. Dual luciferase reporter assay confirmed that miR-199a-5p could directly target DDR1 through binding to its 3′-UTR. Our findings indicated that up-regulation of DDR1 induced by miR-199a-5p down-regulation may contribute to the development and progression of CRC, and this effect may be associated with increased invasiveness, at least in part, via activating the EMT-related signaling.
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         Colorectal cancer (CRC)
         Discoidin domain receptors1 (DDR1)
         MiR-199a-5p
         Metastasis
         Epithelial-to-mesenchymal transition (EMT)
         Gastroenterology
         Hepatology
         Oncology
         Transplant Surgery
         Biochemistry
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