Cancer cells hijack physiologic metabolic signals to seed liver metastasis Editorial


Authors: Rettig, A. R.; Ganesh, K.
Title: Cancer cells hijack physiologic metabolic signals to seed liver metastasis
Abstract: Metastasis arises from cancer cell-intrinsic adaptations and permissive tumor microenvironments (TME) that are distinct across different organs. Deciphering the mechanisms underpinning organotropism could provide novel preventive and therapeutic strategies for patients with cancer. Rogava and colleagues identified Pip4k2c as a driver of liver metastasis, acting by sensitizing cancer cells to insulin-dependent PI3K/AKT signaling, which could be reversed by dual pharmacologic inhibition of PI3K and SGLT2 or a ketogenic diet. The study highlights the importance of tumor microenvironment communication in the context of systemic physiology and points toward potential combination therapies. © 2024 American Association for Cancer Research.
Keywords: signal transduction; protein kinase b; nonhuman; liver neoplasms; biological marker; animal; metabolism; animals; obesity; pathology; phosphatidylinositol 3 kinase; chronic disease; liver metastasis; lung metastasis; cancer cell; liver tumor; diabetes mellitus; proto-oncogene proteins c-akt; metabolic syndrome x; liver parenchyma; cell metabolism; metastatic melanoma; tumor microenvironment; phosphatidylinositol 3-kinases; pi3k/akt signaling; humans; human; article; melanoma cell line; phosphatidylinositol 4 phosphate kinase; physiologic metabolic signal
Journal Title: Cancer Research
Volume: 84
Issue: 10
ISSN: 0008-5472
Publisher: American Association for Cancer Research  
Date Published: 2024-05-15
Start Page: 1548
End Page: 1549
Language: English
DOI: 10.1158/0008-5472.Can-24-0835
PUBMED: 38502849
PROVIDER: scopus
DOI/URL:
Notes: Article -- MSK Cancer Center Support Grant (P30 CA008748) acknowledged in PDF -- MSK corresponding author is Karuna Ganesh -- Source: Scopus
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MSK Authors
  1. Karuna   Ganesh
    68 Ganesh
  2. Andres Rudolf Rettig
    1 Rettig