Cancer: a mirrored room between tumor bulk and tumor microenvironment
Metadata
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Hernández Camarero, Pablo; López Ruiz, Elena; Marchal Corrales, Juan Antonio; Perán, MacarenaEditorial
BMC
Materia
Tumor microenvironment Metastasis Pre-metastatic niche Cancer-associated fibroblasts Tumor-associated macrophages
Date
2021-06-28Referencia bibliográfica
Hernández-Camarero, P... [et al.]. Cancer: a mirrored room between tumor bulk and tumor microenvironment. J Exp Clin Cancer Res 40, 217 (2021). [https://doi.org/10.1186/s13046-021-02022-5]
Sponsorship
FPU grant from the Ministry of Education, Culture and Sport; University of Jaen, Accion I apoyo a la investigacion BIO-349; Junta de Andalucia European Commission SOMM17/6109/UGR; Ministry of Economy and Competitiveness (FEDER) PIE16/00045; Ministry of Science, Innovation and Universities RTI2018-101309-B-C22; Chair "Doctors Galera-Requena in cancer stem cell research" CMC-CTS963Abstract
It has been well documented that the tumor microenvironment (TME) plays a key role in the promotion of drug
resistance, the support of tumor progression, invasiveness, metastasis, and even the maintenance of a cancer stemlike
phenotype. Here, we reviewed TME formation presenting it as a reflection of a tumor’s own organization during
the different stages of tumor development. Interestingly, functionally different groups of stromal cells seem to have
specific spatial distributions within the TME that change as the tumor evolves into advanced stage progression
which correlates with the fact that cancer stem-like cells (CSCs) are located in the edges of solid tumor masses in
advanced tumors.
We also focus on the continuos feedback that is established between a tumor and its surroundings. The “talk”
between tumor mass cells and TME stromal cells, marks the evolution of both interlocuting cell types. For instance,
the metabolic and functional transformations that stromal cells undergo due to tumor corrupting activity.
Moreover, the molecular basis of metastatic spread is also approached, making special emphasis on the site-specific
pre-metastatic niche formation as another reflection of the primary tumor molecular signature.
Finally, several therapeutic approaches targeting primary TME and pre-metastatic niche are suggested. For instance,
a systematic analysis of the TME just adjacent to the tumor mass to establish the proportion of myofibroblasts-like
cancer-associated fibroblasts (CAFs) which may in turn correspond to stemness and metastases-promotion. Or the
implementation of “re-education” therapies consisting of switching tumor-supportive stromal cells into tumorsuppressive
ones. In summary, to improve our clinical management of cancer, it is crucial to understand and learn
how to manage the close interaction between TME and metastasis.