scholarly journals A stroma szerepe a tumorok kialakulásában és progressziójában

2015 ◽  
Vol 156 (45) ◽  
pp. 1816-1823 ◽  
Author(s):  
Marcell Baranyi ◽  
Mónika Lippai ◽  
Zsuzsanna Szatmári

In the last decade, growing attention was paid to the observation that tumors did not only consist of cancer cells, they are rather a complex tissue-like mixture of tumor and stromal cells, which are playing an important role in the course of the malignant disease. Their contribution is so essential that without them, tumors are not even able to grow. This short review summarizes how stromal cells can help the cancerous transformation and early development of tumors, how chronic inflammation contributes to the progression of cancer and how stroma takes part in the induction of angiogenesis. The main mechanisms by which tumors can escape the immune surveillance will be demonstrated as well as the complex contributions of stroma to the invasion, intravasation and metastasis of cancer cells. Finally, possible and promising therapies will be presented that aim at the stroma and its main effects on the progression of tumors. Orv. Hetil., 2015, 156(45), 1816–1823.

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Qi Wu ◽  
Hanpu Zhang ◽  
Si Sun ◽  
Lijun Wang ◽  
Shengrong Sun

AbstractTumor progression requires bidirectional cell-to-cell communication within a complex tumor microenvironment (TME). Extracellular vesicles (EVs) as carriers have the capacity to shuttle regulatory molecules, including nucleic acids, proteins, and lipids, between cancer cells and multiple stromal cells, inducing remarkable phenotypic alterations in the TME. Recently proposed the concept “immunogenic stress”, which means in some stressed microenvironment, cancer cells can release EVs containing specific immunoregulatory mediators, depending on the initiating stress-associated pathway, thereby provoking the changes of immune status in the TME. Considerable evidence has revealed that the intracellular mechanisms underlying the response to diverse stresses are mainly autophagy, endoplasmic reticulum (ER) stress reactions and the DNA damage response (DDR). In addition, the activation of immunogenic stress responses endows hosts with immune surveillance capacity; in contrast, several cargoes in EVs under immunogenic stress trigger a passive immune response by mediating the function of immune cells. This review discusses the current understanding of the immunogenic stress pathways in cancer and describes the interrelation between EVs and immunogenic stress to propose potential treatment strategies and biomarkers.


Metabolites ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 432
Author(s):  
Iván Ponce ◽  
Nelson Garrido ◽  
Nicolás Tobar ◽  
Francisco Melo ◽  
Patricio C. Smith ◽  
...  

Breast tumors belong to the type of desmoplastic lesion in which a stiffer tissue structure is a determinant of breast cancer progression and constitutes a risk factor for breast cancer development. It has been proposed that cancer-associated stromal cells (responsible for this fibrotic phenomenon) are able to metabolize glucose via lactate production, which supports the catabolic metabolism of cancer cells. The aim of this work was to investigate the possible functional link between these two processes. To measure the effect of matrix rigidity on metabolic determinations, we used compliant elastic polyacrylamide gels as a substrate material, to which matrix molecules were covalently linked. We evaluated metabolite transport in stromal cells using two different FRET (Fluorescence Resonance Energy Transfer) nanosensors specific for glucose and lactate. Cell migration/invasion was evaluated using Transwell devices. We show that increased stiffness stimulates lactate production and glucose uptake by mammary fibroblasts. This response was correlated with the expression of stromal glucose transporter Glut1 and monocarboxylate transporters MCT4. Moreover, mammary stromal cells cultured on stiff matrices generated soluble factors that stimulated epithelial breast migration in a stiffness-dependent manner. Using a normal breast stromal cell line, we found that a stiffer extracellular matrix favors the acquisition mechanistical properties that promote metabolic reprograming and also constitute a stimulus for epithelial motility. This new knowledge will help us to better understand the complex relationship between fibrosis, metabolic reprogramming, and cancer malignancy.


2021 ◽  
Vol 26 ◽  
pp. 101031
Author(s):  
Sho Watanabe ◽  
Shuji Hibiya ◽  
Nobuhiro Katsukura ◽  
Sayuki Kitagawa ◽  
Ayako Sato ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3191
Author(s):  
Katherine Po Sin Chung ◽  
Rainbow Wing Hei Leung ◽  
Terence Kin Wah Lee

Cancer stem cells (CSCs) within the tumor bulk play crucial roles in tumor initiation, recurrence and therapeutic resistance. In addition to intrinsic regulation, a growing body of evidence suggests that the phenotypes of CSCs are also regulated extrinsically by stromal cells in the tumor microenvironment (TME). Here, we discuss the current knowledge of the interplay between stromal cells and cancer cells with a special focus on how stromal cells drive the stemness of cancer cells and immune evasive mechanisms of CSCs. Knowledge gained from the interaction between CSCs and stromal cells will provide a mechanistic basis for the development of novel therapeutic strategies for the treatment of cancers.


Lab on a Chip ◽  
2017 ◽  
Vol 17 (16) ◽  
pp. 2852-2860 ◽  
Author(s):  
Qihui Fan ◽  
Ruchuan Liu ◽  
Yang Jiao ◽  
Chunxiu Tian ◽  
James D. Farrell ◽  
...  

A 3-D microfluidic system consisting of microchamber arrays embedded in a collagen hydrogel with tunable biochemical gradients was constructed for investigating interactions between invasive breast cancer cells and stromal cells.


2018 ◽  
Vol 41 (4) ◽  
pp. 353-367 ◽  
Author(s):  
Pritish Nilendu ◽  
Sachin C. Sarode ◽  
Devashree Jahagirdar ◽  
Ishita Tandon ◽  
Shankargouda Patil ◽  
...  

Author(s):  
Madheswaran Suresh ◽  
Malarvizhi Gurusamy ◽  
Natarajan Sudhakar

<p>Immune surveillance is a mechanism where cells and tissues are watched constantly by ever alerted immune system. Most incipient cancer cells are recognized and eliminated by the immune surveillance mechanism, but still tumors have the ability to evade immune surveillance and immunological killing. One greater arm that tumor use to evade immune surveillance, is by expressing anti-phagocytic signal (CD47). Here we present a provocative hypothesis where cancer cells are removed alive by phagocytic cell (DC). That in turn will elicit effective and higher immunogenic condition. All this could be possible by addition pro-phagocytic signal (PtdSer) over cancer cell surface (Breast Cancer), that mask the presence of anti-phagocytic signal (CD47). In other words, adding eat me signal (PtdSer) over the breast cancer cell surface that mask the presence of don’t eat me signal or anti-phagocytic signal present in breast cancer cell surface. This could be possible by using bi-specific antibody, conjugated to PEG-modified liposomes, which carry (PtdSer) pro-phagocytic signal (or) eat me signal, which target both CD47 and EGFRVIII on breast carcinoma. The simultaneous masking of anti-phagocytic signal, and adding of pro–phagocytic signal over cancer cell, will enhance the phagocytic clearance of live tumor cell and elicit immunological killing.</p>


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