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Laminin 521 Modulates the Сytotoxic Effect of 5-Fluorouracil on HT29 Colorectal Cancer Cells

Authors
  • Raigorodskaya, M. P.1
  • Turchinovich, A.2, 3
  • Tsypina, I. M.4, 5
  • Zgoda, V. G.6
  • Nikulin, S. V.1, 7
  • Maltseva, D. V.1, 5
  • 1 Bioclinicum Scientific Research Center, Moscow, 115088, Russia , Moscow (Russia)
  • 2 SciBerg e.Kfm, Mannheim, 68309, Germany , Mannheim (Germany)
  • 3 Molecular Epidemiology C080, German Cancer Research Center, Heidelberg, 69120, Germany , Heidelberg (Germany)
  • 4 Higher School of Economics National Research University, Moscow, 101000, Russia , Moscow (Russia)
  • 5 Shemyakin–Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, 117997, Russia , Moscow (Russia)
  • 6 V.N. Orekhovich Research Institute of Biomedical Chemistry (IBMKh), Russian Academy of Medical Sciences, Moscow, 119121, Russia , Moscow (Russia)
  • 7 Far Eastern Federal University, Vladivostok, 690091, Russia , Vladivostok (Russia)
Type
Published Article
Journal
Applied Biochemistry and Microbiology
Publisher
Pleiades Publishing
Publication Date
Dec 01, 2020
Volume
56
Issue
8
Pages
870–874
Identifiers
DOI: 10.1134/S0003683820080074
Source
Springer Nature
Keywords
License
Yellow

Abstract

AbstractThe cytotoxic effect of 5-fluorouracil (5FU) and regorafenib (RF), drugs with different mechanisms of action used to treat colorectal cancer, on an HT29 cell line cultured on plastic or laminin 521 (LM-521) has been studied. It is first shown that LM-521 can increase the sensitivity of tumor cells to 5FU. A possible mechanism of the observed effect of LM-521 on the HT29 cell viability is proposed based on transcriptome and proteome analysis. The interaction of β1-containing integrins on the cell surface with LM-521 can activate the FAK/PI3K/Akt signaling pathways and promote phosphorylation of the YAP transcription coactivator and its binding to the complex with the 14-3-3σ protein. The formation of this complex leads to YAP retention in the cytoplasm and prevents its transport to the nucleus and the activation of antiapoptotic gene transcription.

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