Gastric Cancer: A Stem Cell Disease?

Giraud, Julie; Bessède, Emilie; Mégraud, Françis; Varon, Christine

doi:10.5772/intechopen.69947

Cited by 2 publications

(2 citation statements)

References 82 publications

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“…This EMT induces emergence of cells with cancer stem cell (CSC) properties [4], characterized by self-renewal and asymmetrical division properties, resistance to conventional therapies (chemo-and radio-therapies), and thus responsible for tumor recurrence and metastasis [6,7], highlighting the importance of targeting these cells. In GC, they express a high level of the cell-surface marker CD44 [5,8,9], a major adhesion molecule for the extracellular matrix. Different variable isoforms exist and have been implicated as key players in malignant transformation.…”

Section: Introductionmentioning

confidence: 99%

Autophagy induced by Helicobacter pylori infection is necessary for gastric cancer stem cell emergence

et al. 2020

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Background The main cause of gastric cancer is the infection by the bacterium Helicobacter pylori which induces a chronic inflammation and an epithelial-to-mesenchymal transition (EMT) leading to the emergence of cells with cancer stem cell (CSC) properties. However, the underlying mechanisms have not been fully characterized. Moreover, H. pylori modulates the host cell autophagic process, but a few studies have investigated the role of this process in tumoral transformation. The aim of this study was to determine whether H. pylori-induced autophagy has a role in CSC emergence. Methods Autophagic flux in response to H. pylori infection was characterized in AGS cell line expressing the tandemtagged mCherry-GFP-LC3 protein and using a ratiometric flow cytometry analysis. Then, AGS and MKN45 cell lines were treated with bafilomycin or chloroquine, two pharmaceutical well-known inhibitors of autophagy, and different EMT and CSC characteristics were analyzed. Results First, a co-expression of the gastric CSC marker CD44 and the autophagic marker LC3 in mice and human stomach tissues infected with H. pylori was observed. Then, we demonstrated in vitro that H. pylori was able to activate the autophagy process with a reduced autophagic flux. Finally, infected cells were treated with autophagy inhibitors, which reduced (i) appearance of mesenchymal phenotypes and migration ability related to EMT and (ii) CD44 expression as well as tumorsphere formation capacities reflecting CSC properties. ConclusionIn conclusion, all these data show that H. pylori-induced autophagy is implicated in gastric CSC emergence and could represent an interesting therapeutic target.

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Section: Introductionmentioning

confidence: 99%

Autophagy induced by Helicobacter pylori infection is necessary for gastric cancer stem cell emergence

et al. 2020

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“…According to the dynamic CSC model, a feedback loop can be established between CSCs and cancer progenitor cells, suggesting that cancer progenitor cells can also acquire stem characteristics under certain microenvironmental cues [14,15]. In this regard, it is becoming clear that inflammatory conditions cooperate to provoke deregulations, mutations, cell fusion and others, ultimately leading CSC promoting conditions [16].…”

Section: Gcsc and The Hierarchical Model Of Tumor Progression: Functi...mentioning

confidence: 99%

The cross talk between gastric cancer stem cells and the immune microenvironment: a tumor-promoting factor

et al. 2021

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Cross talk between cancer cells and the immune system is determinant for cancer progression. Emerging evidence demonstrates that GC characteristics such as metastasis, treatment resistance, and disease recurrence are associated with a tumor subpopulation called gastric cancer stem cells (GCSCs). However, the specific interaction between GCSCs and the immune microenvironment is still under investigation. Although immune evasion has been well described for cancer stem cells (CSCs), recent studies show that GCSCs can also regulate the immune system and even benefit from it. This review will provide an overview of bidirectional interactions between CSCs and immune cells in GC, compiling relevant data about how CSCs can induce leukocyte reprogramming, resulting in pro-tumoral immune cells that orchestrate promotion of metastasis, chemoresistance, tumorigenicity, and even increase in number of cancer cells with stem properties. Some immune cells studied are tumor-associated macrophages (TAMs), neutrophils, Th17 and T regulatory (Treg) cells, mesenchymal stem cells (MSCs), and cancer-associated fibroblasts (CAFs), as well as the signaling pathways involved in these pro-tumoral activities. Conversely, although there are cytotoxic leukocytes that can potentially eliminate GCSCs, we describe mechanisms for immune evasion in GCSCs and their clinical implications. Furthermore, we describe current available immunotherapy targeting GCSC-related markers as possible treatment for GC, discussing how the CSC-modified immune microenvironment can mitigate or inactivate these immunotherapies, limiting their effectiveness. Finally, we summarize key concepts and relevant evidence to understand the cross talk between GCSCs and the immune microenvironment as an important process for effective design of therapies against GCSCs that improve the outcome of patients with GC.

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Gastric Cancer: A Stem Cell Disease?

Cited by 2 publications

References 82 publications

Autophagy induced by Helicobacter pylori infection is necessary for gastric cancer stem cell emergence

Autophagy induced by Helicobacter pylori infection is necessary for gastric cancer stem cell emergence

The cross talk between gastric cancer stem cells and the immune microenvironment: a tumor-promoting factor

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