3
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Investigation of the Effects of Glabridin on the Proliferation, Apoptosis, and Migration of the Human Colon Cancer Cell Lines SW480 and SW620 and Its Mechanism Based on Reverse Virtual Screening and Proteomics

      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

          Colon cancer is a relatively common malignant tumor of the digestive tract. Currently, most colon cancers originate from adenoma carcinogenesis. By screening various licorice flavonoids with anticancer effects, we found that glabridin (GBN) has a prominent anticolon cancer effect. First, we initially explored whether GBN can inhibit proliferation, migration, and invasion and induce apoptosis in SW480 and SW620 cells. Next, we exploited reverse virtual and proteomics technologies to screen out closely related target pathways on the basis of a drug and target database. At the same time, we constructed the structure of the GBN target pathway in colon cancer. We predicted that GBN can regulate the phosphatidylinositol 3-kinase (PI3K)–protein kinase B (AKT)–mammalian target of the rapamycin pathway (mTOR) pathway to fight colon cancer. Finally, through Western blot analysis and qRT-PCR, we verified that the expression levels of the PI3K, AKT, and mTOR proteins and genes in this pathway were significantly reduced after GBN administration. In short, the promising discovery of the anticolon cancer mechanism of GBN provides a reliable experimental basis for subsequent new drug development.

          Related collections

          Most cited references44

          • Record: found
          • Abstract: not found
          • Article: not found

          PI3K: Downstream AKTion Blocks Apoptosis

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Portrait of the PI3K/AKT pathway in colorectal cancer.

            PI3K/AKT signaling leads to reduced apoptosis, stimulates cell growth and increases proliferation. Under normal conditions, PI3K/AKT activation is tightly controlled and dependent on both extracellular growth signals and the availability of amino acids and glucose. Genetic aberrations leading to PI3K/AKT hyper-activation are observed at considerable frequency in all major nodes in most tumors. In colorectal cancer the most commonly observed pathway changes are IGF2 overexpression, PIK3CA mutations and PTEN mutations and deletions. Combined, these alterations are found in about 40% of large bowel tumors. In addition, but not mutually exclusive to these, KRAS mutations are observed at a similar frequency. There are however additional, less frequent and more poorly understood events that may also push the PI3K/AKT pathway into overdrive and thus promote malignant growth. Here we discuss aberrations of components at the genetic, epigenetic, transcriptional, post-transcriptional, translational and post-translational level where perturbations may drive excessive PI3K/AKT signaling. Integrating multiple molecular levels will advance our understanding of this cancer critical circuit and more importantly, improve our ability to pharmacologically target the pathway in view of clonal development, tumor heterogeneity and drug resistance mechanisms. In this review, we revisit the PI3K/AKT pathway cancer susceptibility syndromes, summarize the known aberrations at the different regulatory levels and the prognostic and predictive values of these alterations in colorectal cancer.
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              Progress with proteome projects: why all proteins expressed by a genome should be identified and how to do it.

                Bookmark

                Author and article information

                Contributors
                Journal
                Oxid Med Cell Longev
                Oxid Med Cell Longev
                OMCL
                Oxidative Medicine and Cellular Longevity
                Hindawi
                1942-0900
                1942-0994
                2023
                5 January 2023
                : 2023
                : 1117431
                Affiliations
                1Ningxia Medical University, Yinchuan, Ningxia 750004, China
                2Key Laboratory of Ningxia Minority Medicine Modernization, Ministry of Education (Ningxia Medical University), Yinchuan 750004, China
                Author notes

                Academic Editor: Alessandro Poggi

                Author information
                https://orcid.org/0000-0001-7778-1560
                https://orcid.org/0000-0001-6766-9129
                Article
                10.1155/2023/1117431
                9836797
                36644579
                74072c50-90c9-40a4-aeb8-04d46ee13f25
                Copyright © 2023 Tingting Li et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 21 December 2021
                : 8 October 2022
                : 6 December 2022
                Funding
                Funded by: Ningxia Medical University
                Award ID: XM2020022
                Award ID: XT2022027
                Funded by: National Natural Science Foundation of China
                Award ID: 82160747
                Award ID: 81860708
                Funded by: Ningxia Key Research and Development Program
                Award ID: 2022BSB03081
                Categories
                Research Article

                Molecular medicine
                Molecular medicine

                Comments

                Comment on this article