bims-pimaco Biomed News
on PI3K and MAPK signalling in colorectal cancer
Issue of 2021–12–12
two papers selected by
Lucas B. Zeiger, CRUK Scotland Institute, Beatson Institute for Cancer Research
  1. The Crosstalk Between Signaling Pathways and Cancer Metabolism in Colorectal Cancer.
  2. Oxidative Distress Induces Wnt/β-Catenin Pathway Modulation in Colorectal Cancer Cells: Perspectives on APC Retained Functions.
  1. Front Pharmacol. 2021 ;12 768861
    The Crosstalk Between Signaling Pathways and Cancer Metabolism in Colorectal Cancer.
    Kha Wai Hon, Syafiq Asnawi Zainal Abidin, Iekhsan Othman, Rakesh Naidu.
      Colorectal cancer (CRC) is one of the most frequently diagnosed cancers worldwide. Metabolic reprogramming represents an important cancer hallmark in CRC. Reprogramming core metabolic pathways in cancer cells, such as glycolysis, glutaminolysis, oxidative phosphorylation, and lipid metabolism, is essential to increase energy production and biosynthesis of precursors required to support tumor initiation and progression. Accumulating evidence demonstrates that activation of oncogenes and loss of tumor suppressor genes regulate metabolic reprogramming through the downstream signaling pathways. Protein kinases, such as AKT and c-MYC, are the integral components that facilitate the crosstalk between signaling pathways and metabolic pathways in CRC. This review provides an insight into the crosstalk between signaling pathways and metabolic reprogramming in CRC. Targeting CRC metabolism could open a new avenue for developing CRC therapy by discovering metabolic inhibitors and repurposing protein kinase inhibitors/monoclonal antibodies.
    Keywords:  colorectal cancer; metabolic reprogramming; metabolism; protein kinase; signaling pathways
    DOI:  https://doi.org/10.3389/fphar.2021.768861
  2. Cancers (Basel). 2021 Nov 30. pii: 6045. [Epub ahead of print]13(23):
    Oxidative Distress Induces Wnt/β-Catenin Pathway Modulation in Colorectal Cancer Cells: Perspectives on APC Retained Functions.
    Teresa Catalano, Emira D'Amico, Carmelo Moscatello, Maria Carmela Di Marcantonio, Alessio Ferrone, Giuseppina Bologna, Federico Selvaggi, Paola Lanuti, Roberto Cotellese, Maria Cristina Curia, Rossano Lattanzio, Gitana Maria Aceto.
      Colorectal cancer (CRC) is a multistep process that arises in the colic tissue microenvironment. Oxidative stress plays a role in mediating CRC cell survival and progression, as well as promoting resistance to therapies. CRC progression is associated with Wnt/β-Catenin signaling dysregulation and loss of proper APC functions. Cancer recurrence/relapse has been attributed to altered ROS levels, produced in a cancerous microenvironment. The effect of oxidative distress on Wnt/β-Catenin signaling in the light of APC functions is unclear. This study evaluated the effect of H2O2-induced short-term oxidative stress in HCT116, SW480 and SW620 cells with different phenotypes of APC and β-Catenin. The modulation and relationship of APC with characteristic molecules of Wnt/β-Catenin were assessed in gene and protein expression. Results indicated that CRC cells, even when deprived of growth factors, under acute oxidative distress conditions by H2O2 promote β-Catenin expression and modulate cytoplasmic APC protein. Furthermore, H2O2 induces differential gene expression depending on the cellular phenotype and leading to favor both Wnt/Catenin-dependent and -independent signaling. The exact mechanism by which oxidative distress can affect Wnt signaling functions will require further investigation to reveal new scenarios for the development of therapeutic approaches for CRC, in the light of the conserved functions of APC.
    Keywords:  APC; Wnt/β-Catenin; colorectal cancer; gene expression; microenvironment; oxidative stress; protein expression
    DOI:  https://doi.org/10.3390/cancers13236045
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