The Interaction between Stromal Cells and Tumor Cells

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Stem Cells".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 2604

Special Issue Editors


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Guest Editor
1. i3S–Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal
2. INEB–Instituto de Engenharia Biomédica, Universidade do Porto, 4200-135 Porto, Portugal
3. Departament of Pathology, Faculdade de Medicina, Universidade do Porto, 4200-319 Porto, Portugal
Interests: tumor microenvironment; tumor immunology; colorectal cancer; radiotherapy

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Guest Editor
Epithelial Interactions in Cancer Group, i3S - Instituto de Investigação e Inovação em Saúde da Universidade do Porto, IPATIMUP - Institute of Molecular Pathology and Immunology, University of Porto, Porto, Portugal
Interests: Oncobiology; Oncogenic signalling; KRAS; Tumor microenvironment; Cancer-associated fibroblasts; Therapy resistance; Cell communication; Cell signalling

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Guest Editor
Epithelial Interactions in Cancer Group, Ipatimup - Institute of Molecular Pathology and Immunology of University of Porto, i3S - Institute for Research and Innovation in Health, University of Porto, Porto, Portugal
Interests: Extracellular Vesicles; Gastrointestinal Cancers; Cancer genetics/epigenetics

Special Issue Information

Dear Colleagues,

Genetic and epigenetic alterations that activate oncogenes or inactivate tumor suppressor genes have been considered for a long time to be the main drivers of cancer development and progression. Yet, the dynamic interactions established between cancer cells and the cellular and non-cellular components of their tumor microenvironment—the stromal components—are now acknowledged as an essential modulator of cancer cell malignant traits. Actually, these interactions activate various pro-tumor pathways that regulate vital processes such as growth, survival, stemness, migration, invasion, metastization, and metabolic reprogramming, thus negatively impacting therapy responses and actively inducing mechanisms of therapy resistance.

This Special Issue aims to provide a comprehensive overview on the role of cancer cell–stromal interactions on tumor initiation, progression and therapy resistance. We kindly invite you to share your studies presenting novel ideas and perspectives, as well as novel methodologies and technology developments, to address cancer cell–stromal interactions from a molecular and mechanistic standpoint. We welcome studies addressing the different aspects of cancer cell–stromal interactions, such as:

  • How cancer cells with different genetic alterations affect the stromal composition and its pro-tumor properties;
  • How stromal-derived signals shape the genetic and epigenetic landscape of cancer cells;
  • How cancer cell–stromal interactions evolve from tumor initiation to metastization;
  • Which communication routes are implicated (e.g., direct contact, soluble factors, exosomes, tunneling nanotubes);
  • How therapy shapes and reprograms the stromal components and how these impact therapy resistance mechanisms;
  • Identification of novel disease biomarkers derived from the crosstalk between cancer cells and stromal components;
  • Identification and development of novel therapies targeting cancer cell–stromal interactions.

We are looking forward to your contributions!

Prof. Dr. Maria José Cardoso Oliveira
Dr. Sérgia Velho
Dr. Joana Carvalho
Guest Editors

Manuscript Submission Information

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Keywords

  • oncogenes
  • cancer development
  • cancer cells
  • tumor microenvironment
  • stromal components
  • tumor initiation

Published Papers (1 paper)

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Research

14 pages, 2068 KiB  
Article
Modulation of Fibroblast Phenotype by Colorectal Cancer Cell-Secreted Factors Is Mostly Independent of Oncogenic KRAS
by Patrícia Dias Carvalho, Susana Mendonça, Flávia Martins, Maria José Oliveira and Sérgia Velho
Cells 2022, 11(16), 2490; https://doi.org/10.3390/cells11162490 - 11 Aug 2022
Cited by 2 | Viewed by 2113
Abstract
KRAS mutations have been shown to extend their oncogenic effects beyond the cancer cell, influencing the tumor microenvironment. Herein, we studied the impact of mutant KRAS on the modulation of the pro-tumorigenic properties of cancer-associated fibroblasts (CAFs), including α-SMA expression, TGFβ1 and HGF [...] Read more.
KRAS mutations have been shown to extend their oncogenic effects beyond the cancer cell, influencing the tumor microenvironment. Herein, we studied the impact of mutant KRAS on the modulation of the pro-tumorigenic properties of cancer-associated fibroblasts (CAFs), including α-SMA expression, TGFβ1 and HGF production, extracellular matrix components and metalloproteinases expression as well as collagen contraction and migration capacities. To do so, CCD-18Co normal-like colon fibroblasts were challenged with conditioned media from control and KRAS silenced colorectal cancer (CRC) cells. Our results showed that the mutant KRAS CRC cell-secreted factors were capable of turning normal-like fibroblasts into CAF-like by modulating the α-SMA expression, TGFβ1 and HGF production and migration capacity. Oncogenic KRAS played a secondary role as its silencing did not completely impair the capacity of CRC cells to modulate most of the fibroblast properties analyzed. In summary, our work suggests that mutant KRAS does not play a major role in controlling the CRC cell-secreted factors that modulate the behavior of fibroblasts. The fact that CRC cells retain the capacity to modulate the pro-tumorigenic features of fibroblasts independently of KRAS silencing is likely to negatively impact their response to KRAS inhibitors, thus standing as a putative mechanism of resistance to KRAS inhibition with potential therapeutical relevance. Full article
(This article belongs to the Special Issue The Interaction between Stromal Cells and Tumor Cells)
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