The normal cells of the organ support the metabolic adaptation of tumors

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The normal cells of the organ support the metabolic adaptation of tumors

Tuesday, 14.03.2017

Tumor growth is dependent on the ability of malignant cells to survive in the microenvironment of the organ where it develops. Normal cells in the tumor microenvironment contribute for this adaptative process by sharing soluble factors and organic molecules that meet the energetic and biomass requirements of the tumor.

In this scientific paper, we show the role of fibroblasts in the metabolism of fatty acids in breast cancer. In in vitro and in vivo models, it has been shown that tumor associated fibroblasts provide fatty acids to tumor cells, contributing for tumor growth. The Fatty Acid Transporter Protein 1 (FATP1) seems to play a key role in this metabolic dialogue and is being further investigated to verify the viability of its use as a therapeutic target.


Authors and Affiliations:

Filipa Lopes-Coelhoa,b1, Saudade Andréa,c1, Ana Félixa,c, Jacinta Serpaa,b

aCentro de Estudos de Doenças Crónicas (CEDOC), NOVA Medical School/Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Campo Mártires da Pátria 130, 1169-056, Lisboa, Portugal

bUnidade de Investigação Em Patobiologia Molecular Do Instituto Português de Oncologia de Lisboa Francisco Gentil (IPOLFG), Rua Prof Lima Basto, 1099-023, Lisboa, Portugal

cServiço de Anatomia Patológica, IPOLFG, Rua Prof Lima Basto, 1099-023, Lisboa, Portugal



The cellular components of microenvironment are partners of cancer cells, sharing soluble factors and organic molecules to accomplish tumor energy and biomass demands. We tested the role of fibroblasts in fatty acids metabolism in breast cancer, addressing fatty acid synthase (FASN) expression and activity, the expression of lipids chaperons (FABPs) and transporters (FATPs) and lipids cellular content.

We showed that the amount of lipids increased in cancer cells exposed to fibroblasts conditioned media, showing that lipids transfer is crucial in this metabolic cross-talk. Accordingly, it was seen in those cancer cells a concomitant decrease in the expression of FABP2 and FABP3 and an increase in FATP1 expression, whose function is independent of FABPs. The in vivo experiment corroborates the role of CAFs in tumor growth.

Our study is one more step toward the understanding of metabolic dynamics between cancer cells and CAFs, disclosing FATP1 as a putative target to disturb the transfer of lipids between CAFs and breast cancer cells.


Journal: Molecular and Cellular Endocrinology




Legend of the photo:

Cancer associated fibroblasts (CAFs) produce lipids to supply breast cancer cells (BCCs). CAFs exhibit high levels of fatty acid synthase (FASN) activity and lipids production; lipids are secreted through the FATP1 and CD36. The influence of CAFs and the high levels of lipids in the external media induce a metabolic switch in BCCs from producers to gatherers of lipids, by decreasing the activity of FASN and giving a pivotal role to FATP1 as a lipids transporter.