23
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Luteolin suppresses colorectal cancer cell metastasis via regulation of the miR-384/pleiotrophin axis

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Luteolin (3,4,5,7-tetrahydroxyflavone) is a natural flavonoid that has been found to exhibit anticancer properties in certain types of cancers. In the present study, the role of luteolin and its underlying mechanisms were explored in colorectal cancer (CRC) cells. First, the effects of luteolin on CRC cells proliferation, migration and invasion were examined by CCK-8, wound healing and Transwell assays, respectively. It was demonstrated that luteolin had no effects on CRC cells proliferation while inhibited cells migration and invasion both in vitro and in vivo. Then, expression of pleiotrophin (PTN) and miR-384 was detected in cells and CRC tissues by qPCR. Luteolin was found to upregulate miR-384 and downregulate PTN expressions both in CRC cells and tissues. miR-384 inhibition and PTN overexpression partially reversed the inhibition of HT-29 cells migration and invasion induced by luteolin. Target analysis revealed that miR-384 directly regulates PTN expression. The correlation analysis between PTN expression and clinical characteristics revealed that PTN expression was positively related to cancer progression. The present study demonstrated that luteolin exerts anticancer effects against CRC cells by modulating PTN via miR-384 expression suggested that PTN may serve as a promising candidate for therapeutic applications in CRC treatment.

          Related collections

          Most cited references32

          • Record: found
          • Abstract: found
          • Article: not found
          Is Open Access

          CRNDE Promotes Malignant Progression of Glioma by Attenuating miR-384/PIWIL4/STAT3 Axis.

          Colorectal neoplasia differentially expressed (CRNDE) is the most upregulated long noncoding RNA (lncRNA) in glioma. Herein, the function and potential molecular mechanisms of CRNDE and miR-384 were illustrated in glioma cells. CRNDE overexpression facilitated cell proliferation, migration, and invasion, while inhibited glioma cells apoptosis. Quantitative real-time polymerase chain reaction (PCR) demonstrated that miR-384 was downregulated in human glioma tissues and glioma cell lines. Moreover, restoration of miR-384 exerted tumor-suppressive functions. In addition, the expression of miR-384 was negatively correlated with CRNDE expression. A binding region between CRNDE and miR-384 was confirmed using luciferase assays. Moreover, CRNDE promoted cell malignant behavior by decreasing miR-384 expression. At the molecular level, treatment by CRNDE knockdown or miR-384 overexpression resulted in a decrease of piwi-like RNA-mediated gene silencing 4 (PIWIL4) protein. Besides, PIWIL4 was identified as a target of miR-384 and plays an oncogenic role in glioma. Similarly, downstream proteins of PIWIL4 such as STAT3, cyclin D1, VEGFA, SLUG, MMP-9, caspase 3, Bcl-2, and bcl-xL were modulated when treated with miR-384 and PIWIL4. Remarkably, CRNDE knockdown combined with miR-384 overexpression led to tumor regression in vivo. Overall, these results depicted a novel pathway mediated by CRNDE in glioma, which may be a potential application for glioma therapy.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Midkine and pleiotrophin: two related proteins involved in development, survival, inflammation and tumorigenesis.

            Midkine (MK) and pleiotrophin (PTN) are low molecular weight proteins with closely related structures. They are mainly composed of two domains held by disulfide bridges, and there are three antiparallel beta-sheets in each domain. MK and PTN promote the growth, survival, and migration of various cells, and play roles in neurogenesis and epithelial mesenchymal interactions during organogenesis. A chondroitin sulfate proteoglycan, protein-tyrosine phosphatase zeta (PTPzeta), is a receptor for MK and PTN. The downstream signaling system includes ERK and PI3 kinase. MK binds to the chondroitin sulfate portion of PTPzeta with high affinity. Among the various chondroitin sulfate structures, the E unit, which has 4,6-disulfated N-acetylgalactosamine, provides the strongest binding site. The expression of MK and PTN is increased in various human tumors, making them promising as tumor markers and as targets for tumor therapy. MK and PTN expression also increases upon ischemic injury. MK enhances the migration of inflammatory cells, and is involved in neointima formation and renal injury following ischemia. MK is also interesting from the viewpoints of the treatment of neurodegenerative diseases, increasing the efficiency of in vitro development, and the prevention of HIV infection.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              LncRNA CRNDE promotes hepatic carcinoma cell proliferation, migration and invasion by suppressing miR-384.

              Studies have found that colorectal neoplasia differentially expressed (CRNDE) is related to cancer development. Herein, we found that the expression of CRNDE was increased in human hepatic carcinoma (HCC) tissues and cell lines. The ROC curve analysis illustrated CRNDE has a significant diagnostic value for HCC. At the same time, CRNDE promotes HCC cell proliferation, migration, and invasionin vitro. Quantitative real-time polymerase chain reaction (PCR) demonstrated that miR-384 was significantly downregulated in HCC tissues. Moreover, we indicated CRNDE negatively regulated miR-384 expression in HCC. In addition, we found that CRNDE accelerated the expression levels of NF-κB and p-AKT though inhibition of miR-384. Overall, these results suggested that CRNDE-miR-384 axis might be a promising therapeutic target for the treatment of HCC.
                Bookmark

                Author and article information

                Journal
                Oncol Rep
                Oncol. Rep
                Oncology Reports
                D.A. Spandidos
                1021-335X
                1791-2431
                July 2019
                24 April 2019
                24 April 2019
                : 42
                : 1
                : 131-141
                Affiliations
                [1 ]Department of Colorectal Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310003, P.R. China
                [2 ]Department of Colorectal Surgery, Hangzhou Hospital of Traditional Chinese Medicine, Guangxing Hospital Affiliated to Zhejiang University of Traditional Chinese Medicine, Hangzhou, Zhejiang 310003, P.R. China
                [3 ]Department of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, P.R. China
                Author notes
                Correspondence to: Dr Saisai Wang, Department of Colorectal Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou, Zhejiang 310003, P.R. China, E-mail: saisaiwang@ 123456zju.edu.cn
                Article
                or-42-01-0131
                10.3892/or.2019.7136
                6549074
                31059061
                fc680137-43a5-4b77-bc63-bdcd13413b05
                Copyright: © Yao et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 01 November 2018
                : 03 April 2019
                Categories
                Articles

                luteolin,colorectal cancer,mir-384,ptn,invasion,metastasis
                luteolin, colorectal cancer, mir-384, ptn, invasion, metastasis

                Comments

                Comment on this article