Control of Metastasis by NK Cells

Alejandro López-Soto, Segundo Gonzalez, Mark J. Smyth, Lorenzo Galluzzi

Research output: Contribution to journalReview articlepeer-review

548 Scopus citations

Abstract

The metastatic spread of malignant cells to distant anatomical locations is a prominent cause of cancer-related death. Metastasis is governed by cancer-cell-intrinsic mechanisms that enable neoplastic cells to invade the local microenvironment, reach the circulation, and colonize distant sites, including the so-called epithelial-to-mesenchymal transition. Moreover, metastasis is regulated by microenvironmental and systemic processes, such as immunosurveillance. Here, we outline the cancer-cell-intrinsic and -extrinsic factors that regulate metastasis, discuss the key role of natural killer (NK) cells in the control of metastatic dissemination, and present potential therapeutic approaches to prevent or target metastatic disease by harnessing NK cells. The metastatic spread of malignant cells to distant anatomical locations is a prominent cause of cancer-related death. Metastasis is governed by cancer-cell-intrinsic mechanisms that enable neoplastic cells to invade the local microenvironment, reach the circulation, and colonize distant sites, including the so-called epithelial-to-mesenchymal transition. Moreover, metastasis is regulated by microenvironmental and systemic processes, such as immunosurveillance. Here, we outline the cancer-cell-intrinsic and -extrinsic factors that regulate metastasis, discuss the key role of natural killer (NK) cells in the control of metastatic dissemination, and present potential therapeutic approaches to prevent or target metastatic disease by harnessing NK cells.

Original languageEnglish
Pages (from-to)135-154
Number of pages20
JournalCancer Cell
Volume32
Issue number2
DOIs
StatePublished - Aug 14 2017
Externally publishedYes

Keywords

  • ADCC
  • circulating tumor cells
  • CTLA4
  • disseminated tumor cells
  • DNAM-1
  • immune checkpoint blockers
  • metastatic cascade
  • NKG2D
  • PD-1
  • TGFB1

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