SEMA4D Knockdown Attenuates β-Catenin-Dependent Tumor Progression in Colorectal Cancer.

Semaphorin 4D (SEMA4D), a protein originally demonstrated to regulate the immune system and axonal growth cone collapse in the developing central nervous system, is overexpressed in various human malignancies, including colorectal cancer (CRC). This investigation was undertaken to examine the effect...

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Published in:BioMed Research International pp. 1 - 13
Main Authors: Rezaeepoor, Mahsa, Rashidi, Golnaz, Pourjafar, Mona, Mohammadi, Chiman, Solgi, Ghasem, Najafi, Rezvan
Format: pictorial research tables/charts Journal Article
Published: Wiley-Blackwell 7/22/2021
Online Access:View this record in EBSCOhost
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      jtl: BioMed Research International
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      dt: 7/22/2021
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1155/2021/8507373
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        atl: SEMA4D Knockdown Attenuates β-Catenin-Dependent Tumor Progression in Colorectal Cancer.
      aug:
        au:
          Rezaeepoor, Mahsa
          Rashidi, Golnaz
          Pourjafar, Mona
          Mohammadi, Chiman
          Solgi, Ghasem
          Najafi, Rezvan
        affil: Department of Immunology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
      sug:
        subj:
          Colorectal Neoplasms
          Disease Progression
          Proteins
          Apoptosis
          Caspases
          Human
          Stem Cells
      ab: Semaphorin 4D (SEMA4D), a protein originally demonstrated to regulate the immune system and axonal growth cone collapse in the developing central nervous system, is overexpressed in various human malignancies, including colorectal cancer (CRC). This investigation was undertaken to examine the effects of SEMA4D silencing on the biological properties of the CRC cell line. SW48 cells were transfected with a siRNA-targeting SEMA4D. The mRNA expression of underlying pro- and antiapoptotic proteins including Bax, Bcl-2, P53, and caspase-3, cancer stem cell (CSC) markers, epithelial-mesenchymal transition (EMT) markers, MMP-2, and MMP-9 was examined using qRT-PCR. Further, the protein expression of E-cadherin and β-catenin was confirmed by Western blot. SW48 cell migration and MMP activity were detected using scratch and zymography analysis, respectively. Finally, the apoptosis rate was assessed via the flowcytometry test. SEMA4D knock-down was associated with a considerable suppression of in vitro cell viability, EMT-related genes, CSC markers, β-catenin signaling pathway, sphere-forming, cell migration, and MMP-2 activity as well as induction of apoptosis. This study identifies the inhibitory effects of SEMA4D gene silencing on tumor progression. Thereby, this might conclude a possible alternative to cancer therapy by targeting several prominent pathways involved in cancer through SEMA4D suppression.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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