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EMT and inflammation: inseparable actors of cancer progression
#MMPMID28599100
Suarez-Carmona M
; Lesage J
; Cataldo D
; Gilles C
Mol Oncol
2017[Jul]; 11
(7
): 805-823
PMID28599100
show ga
Tumors can be depicted as wounds that never heal, and are infiltrated by a large
array of inflammatory and immune cells. Tumor-associated chronic inflammation is
a hallmark of cancer that fosters progression to a metastatic stage, as has been
extensively reviewed lately. Indeed, inflammatory cells persisting in the tumor
establish a cross-talk with tumor cells that may result in a phenotype switch
into tumor-supporting cells. This has been particularly well described for
macrophages and is referred to as tumor-associated 'M2' polarization.
Epithelial-to-mesenchymal transition (EMT), the embryonic program that loosens
cell-cell adherence complexes and endows cells with enhanced migratory and
invasive properties, can be co-opted by cancer cells during metastatic
progression. Cancer cells that have undergone EMT are more aggressive, displaying
increased invasiveness, stem-like features, and resistance to apoptosis. EMT
programs can also stimulate the production of proinflammatory factors by cancer
cells. Conversely, inflammation is a potent inducer of EMT in tumors. Therefore,
the two phenomena may sustain each other, in an alliance for metastasis. This is
the focus of this review, where the interconnections between EMT programs and
cellular and molecular actors of inflammation are described. We also recapitulate
data linking the EMT/inflammation axis to metastasis.
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