scholarly journals The Crosstalk between Cancer Stem Cells and Microenvironment Is Critical for Solid Tumor Progression: The Significant Contribution of Extracellular Vesicles

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Chiara Ciardiello ◽  
Alessandra Leone ◽  
Alfredo Budillon
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Tumor Progression ◽  
Cell Fate ◽  
Extracellular Vesicles ◽  
Significant Contribution ◽  
Critical Role ◽  
Mediated Communication

Several evidences nowadays demonstrated the critical role of the microenvironment in regulating cancer stem cells and their involvement in tumor progression. Extracellular vesicles (EVs) are considered as one of the most effective vehicles of information among cells. Accordingly, a number of studies led to the recognition of stem cell-associated EVs as new complexes able to contribute to cell fate determination of either normal or tumor cells. In this review, we aim to highlight an existing bidirectional role of EV-mediated communication—from cancer stem cells to microenvironment and also from microenvironment to cancer stem cells—in the most widespread solid cancers as prostate, breast, lung, and colon tumors.

scholarly journals Extracellular Vesicles and Cancer Stem Cells in Tumor Progression: New Therapeutic Perspectives

2021 ◽  
Vol 22 (19) ◽  
pp. 10572
Author(s):  
Maria Giovanna Scioli ◽  
Sonia Terriaca ◽  
Elena Fiorelli ◽  
Gabriele Storti ◽  
Giulia Fabbri ◽  
...  
Keyword(s):  
Stem Cells ◽  
Drug Resistance ◽  
Cancer Stem Cells ◽  
Tumor Growth ◽  
Tumor Progression ◽  
Extracellular Vesicles ◽  
Cross Talk ◽  
Cell Populations ◽  
Disease Relapse

Tumor burden is a complex microenvironment where different cell populations coexist and have intense cross-talk. Among them, a heterogeneous population of tumor cells with staminal features are grouped under the definition of cancer stem cells (CSCs). CSCs are also considered responsible for tumor progression, drug resistance, and disease relapse. Furthermore, CSCs secrete a wide variety of extracellular vesicles (EVs) with different cargos, including proteins, lipids, ssDNA, dsDNA, mRNA, siRNA, or miRNA. EVs are internalized by other cells, orienting the microenvironment toward a protumorigenic and prometastatic one. Given their importance in tumor growth and metastasis, EVs could be exploited as a new therapeutic target. The inhibition of biogenesis, release, or uptake of EVs could represent an efficacious strategy to impair the cross-talk between CSCs and other cells present in the tumor microenvironment. Moreover, natural or synthetic EVs could represent suitable carriers for drugs or bioactive molecules to target specific cell populations, including CSCs. This review will discuss the role of CSCs and EVs in tumor growth, progression, and metastasis and how they affect drug resistance and disease relapse. Furthermore, we will analyze the potential role of EVs as a target or vehicle of new therapies.

scholarly journals MicroRNA-28-5p Regulates Liver Cancer Stem Cell Expansion via IGF-1 Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Qing Xia ◽  
Tao Han ◽  
Pinghua Yang ◽  
Ruoyu Wang ◽  
Hengyu Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Critical Role ◽  
Self Renewal ◽  
Sorafenib Treatment ◽  
The Impact

Background. MicroRNAs (miRNAs) play a critical role in the regulation of cancer stem cells (CSCs). However, the role of miRNAs in liver CSCs has not been fully elucidated. Methods. Real-time PCR was used to detect the expression of miR-miR-28-5p in liver cancer stem cells (CSCs). The impact of miR-28-5p on liver CSC expansion was investigated both in vivo and in vitro. The correlation between miR-28-5p expression and sorafenib benefits in HCC was further evaluated in patient-derived xenografts (PDXs). Results. Our data showed that miR-28-5p was downregulated in sorted EpCAM- and CD24-positive liver CSCs. Biofunctional investigations revealed that knockdown miR-28-5p promoted liver CSC self-renewal and tumorigenesis. Consistently, miR-28-5p overexpression inhibited liver CSC’s self-renewal and tumorigenesis. Mechanistically, we found that insulin-like growth factor-1 (IGF-1) was a direct target of miR-28-5p in liver CSCs, and the effects of miR-28-5p on liver CSC’s self-renewal and tumorigenesis were dependent on IGF-1. The correlation between miR-28-5p and IGF-1 was confirmed in human HCC tissues. Furthermore, the miR-28-5p knockdown HCC cells were more sensitive to sorafenib treatment. Analysis of patient-derived xenografts (PDXs) further demonstrated that the miR-28-5p may predict sorafenib benefits in HCC patients. Conclusion. Our findings revealed the crucial role of the miR-28-5p in liver CSC expansion and sorafenib response, rendering miR-28-5p an optimal therapeutic target for HCC.

The Distinct Role of Extracellular Vesicles Derived from Normal and Cancer Stem Cells

2017 ◽  
Vol 3 (3) ◽  
pp. 218-224 ◽  
Author(s):  
Cristina Grange ◽  
Marta Tapparo ◽  
Sharad Kholia ◽  
Benedetta Bussolati ◽  
Giovanni Camussi
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Extracellular Vesicles ◽  
Distinct Role

scholarly journals The Contributions of Prostate Cancer Stem Cells in Prostate Cancer Initiation and Metastasis

Cancers ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 434 ◽  
Author(s):  
Wenjuan Mei ◽  
Xiaozeng Lin ◽  
Anil Kapoor ◽  
Yan Gu ◽  
Kuncheng Zhao ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Epithelial Mesenchymal Transition ◽  
Critical Role ◽  
Current Evidence ◽  
Target Cells ◽  
Mesenchymal Transition ◽  
Prostate Cancer Stem Cells

Research in the last decade has clearly revealed a critical role of prostate cancer stem cells (PCSCs) in prostate cancer (PC). Prostate stem cells (PSCs) reside in both basal and luminal layers, and are the target cells of oncogenic transformation, suggesting a role of PCSCs in PC initiation. Mutations in PTEN, TP53, and RB1 commonly occur in PC, particularly in metastasis and castration-resistant PC. The loss of PTEN together with Ras activation induces partial epithelial–mesenchymal transition (EMT), which is a major mechanism that confers plasticity to cancer stem cells (CSCs) and PCSCs, which contributes to metastasis. While PTEN inactivation leads to PC, it is not sufficient for metastasis, the loss of PTEN concurrently with the inactivation of both TP53 and RB1 empower lineage plasticity in PC cells, which substantially promotes PC metastasis and the conversion to PC adenocarcinoma to neuroendocrine PC (NEPC), demonstrating the essential function of TP53 and RB1 in the suppression of PCSCs. TP53 and RB1 suppress lineage plasticity through the inhibition of SOX2 expression. In this review, we will discuss the current evidence supporting a major role of PCSCs in PC initiation and metastasis, as well as the underlying mechanisms regulating PCSCs. These discussions will be developed along with the cancer stem cell (CSC) knowledge in other cancer types.

Role of Geminin in cell fate determination of hematopoietic stem cells (HSCs)

2016 ◽  
Vol 104 (3) ◽  
pp. 324-329 ◽  
Author(s):  
Shin’ichiro Yasunaga ◽  
Yoshinori Ohno ◽  
Naoto Shirasu ◽  
Bo Zhang ◽  
Kyoko Suzuki-Takedachi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Cell Fate ◽  
Cell Fate Determination ◽  
Hematopoietic Stem ◽  
Fate Determination

The critical role of SDF-1/CXCR4 axis in cancer and cancer stem cells metastasis

2008 ◽  
Vol 31 (9) ◽  
pp. 809-819 ◽  
Author(s):  
S. Gelmini ◽  
M. Mangoni ◽  
M. Serio ◽  
P. Romagnani ◽  
E. Lazzeri
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Critical Role ◽  
Cxcr4 Axis

scholarly journals Mesenchymal Stem Cells and Extracellular Vesicles in Osteosarcoma Pathogenesis and Therapy

2021 ◽  
Vol 22 (20) ◽  
pp. 11035
Author(s):  
Virinder Kaur Sarhadi ◽  
Ravindra Daddali ◽  
Riitta Seppänen-Kaijansinkko
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Extracellular Vesicles ◽  
Poor Prognosis ◽  
Paracrine Signaling ◽  
Mediated Communication ◽  
Multipotent Stem Cells ◽  
Genetic Complexity ◽  
Potential Applications

Osteosarcoma (OS) is an aggressive bone tumor that mainly affects children and adolescents. OS has a strong tendency to relapse and metastasize, resulting in poor prognosis and survival. The high heterogeneity and genetic complexity of OS make it challenging to identify new therapeutic targets. Mesenchymal stem cells (MSCs) are multipotent stem cells that can differentiate into adipocytes, osteoblasts, or chondroblasts. OS is thought to originate at some stage in the differentiation process of MSC to pre-osteoblast or from osteoblast precursors. MSCs contribute to OS progression by interacting with tumor cells via paracrine signaling and affect tumor cell proliferation, invasion, angiogenesis, immune response, and metastasis. Extracellular vesicles (EVs), secreted by OS cells and MSCs in the tumor microenvironment, are crucial mediators of intercellular communication, driving OS progression by transferring miRNAs/RNA and proteins to other cells. MSC-derived EVs have both pro-tumor and anti-tumor effects on OS progression. MSC-EVs can be also engineered to deliver anti-tumor cargo to the tumor site, which offers potential applications in MSC-EV-based OS treatment. In this review, we highlight the role of MSCs in OS, with a focus on EV-mediated communication between OS cells and MSCs and their role in OS pathogenesis and therapy.

scholarly journals CD147 Promotes Cell Small Extracellular Vesicles Release during Colon Cancer Stem Cells Differentiation and Triggers Cellular Changes in Recipient Cells

Cancers ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 260 ◽  
Author(s):  
Donatella Lucchetti ◽  
Filomena Colella ◽  
Luigi Perelli ◽  
Claudio Ricciardi-Tenore ◽  
Federica Calapà ◽  
...  
Keyword(s):  
Stem Cells ◽  
Colon Cancer ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Extracellular Vesicles ◽  
Multivesicular Body ◽  
Cellular Changes ◽  
Colon Cancer Stem Cells ◽  
Colorectal Cancer Stem Cells

Cancer cells secrete small extracellular vesicles (sEVs) that are involved in the remodeling of tumor microenvironment (TME) and can promote tumor progression. The role of sEVs and their molecular key players in colon cancer stem cells differentiation are poorly understood. This study aimed to analyze the role and content of sEVs released during the differentiation of colorectal cancer stem cells. Here we show that sEVs secretion during colon cancer stem cells differentiation is partially controlled by CD147, a well-known player involved in colon cancer tumorigenesis. CD147 + sEVs activate a signaling cascade in recipient cells inducing molecular invasive features in colon cancer cells. CD147 knockdown as well as anti-CD147 antibodies impaired sEVs release and downstream effects on recipient cells and blocking multivesicular body maturation prevented sEVs release during the differentiation. Our findings reveal a functional role of CD147 in promoting sEVs release during the differentiation of colon cancer stem cells and in triggering cellular changes in recipient cells.

Role of Nrf2 and mitochondria in cancer stem cells; in carcinogenesis, tumor progression, and chemoresistance

Biochimie ◽  
2020 ◽  
Vol 179 ◽  
pp. 32-45 ◽  
Author(s):  
Zahra Payandeh ◽  
Abbas Pirpour Tazehkand ◽  
Ghasem Barati ◽  
Farhad Pouremamali ◽  
Houman Kahroba ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Tumor Progression

scholarly journals The role of cancer stem cells in glioblastoma

2014 ◽  
Vol 37 (6) ◽  
pp. E6 ◽  
Author(s):  
Swetha J. Sundar ◽  
Jason K. Hsieh ◽  
Sunil Manjila ◽  
Justin D. Lathia ◽  
Andrew Sloan
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Model ◽  
Critical Role ◽  
Treatment Resistance ◽  
Molecular Heterogeneity ◽  
Clinical Investigations ◽  
Stem Cell Model ◽  
Cancer Stem Cell Model

Recurrence in glioblastoma is nearly universal, and its prognosis remains dismal despite significant advances in treatment over the past decade. Glioblastoma demonstrates considerable intratumoral phenotypic and molecular heterogeneity and contains a population of cancer stem cells that contributes to tumor propagation, maintenance, and treatment resistance. Cancer stem cells are functionally defined by their ability to self-renew and to differentiate, and they constitute the diverse hierarchy of cells composing a tumor. When xenografted into an appropriate host, they are capable of tumorigenesis. Given the critical role of cancer stem cells in the pathogenesis of glioblastoma, research into their molecular and phenotypic characteristics is a therapeutic priority. In this review, the authors discuss the evolution of the cancer stem cell model of tumorigenesis and describe the specific role of cancer stem cells in the pathogenesis of glioblastoma and their molecular and microenvironmental characteristics. They also discuss recent clinical investigations into targeted therapies against cancer stem cells in the treatment of glioblastoma.

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