The correlation of hematopoietic stem cells with cancer stem cells through the regulation of stromal cells in tumor microenvironment

Lin, Shuchen; Fu, Shanlin

doi:10.1016/j.mehy.2012.12.016

Cited by 3 publications

(3 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tumor stromal hematopoietic cells do originate from BM, and may be recruited to tumor sites from the peripheral blood through inflammatory signals [20][21][22]. HSCs have been previously indicated as a compartment of tumor stroma; moreover, it has been hypothesized that HSCs can be taught by the primary tumor to favor metastatic spreading [23]. Here, we demonstrated that pharmacological antagonism of β3-AR by using SR59230A induced a multi-lineage commitment of the HSCs recruited in the tumor microenvironment, and partially in the bone marrow niche, and that this effect impairs stromal cells sustainability to tumor progression.…”

Section: Discussionmentioning

confidence: 99%

β3-Adrenoreceptor Blockade Induces Stem Cells Differentiation in Melanoma Microenvironment

Calvani

Bruno

Dabraio

et al. 2020

IJMS

View full text Add to dashboard Cite

Although there is an increasing evidence that cancer stem cell (CSC) niches in the tumor microenvironment (TME) plays a crucial role in sustaining solid tumors progression, several molecular players involved in this regulation still remain unknown. The role of β-adrenergic signaling in enhancing tumor growth through β2-adrenoreceptors (β2-ARs) has been confirmed in different cancer models, but the role played by the β3-adrenergic receptor (β3-AR) has recently emerged. Previous studies showed that β3-AR promotes cancer growth through the activation of different stromal cells in the TME, and leads to melanoma malignancy progression through inflammation, angiogenesis, and immunotolerance. Here we show that in B16 melanoma-bearing mice, the pharmacological β3-AR blockade is able to reduce the expression of CSC markers, and to induce a differentiated phenotype of hematopoietic subpopulations in TME. In particular, cytofluorimetric analysis (FACS) of the tumor mass shows that β3-AR antagonist SR59230A promotes hematopoietic differentiation as indicated by increased ratios of lymphoid/hematopoietic stem cells (HSCs) and of myeloid progenitor cells/HSCs, and increases the number of Ter119 and natural killer (NK) precursor cells, and of granulocyte precursors, indicating active hematopoiesis within the tumor tissue. Moreover, pharmacological antagonism of β3-AR induces mesenchymal stem cell (MSC) differentiation into adipocytes subtracting a potential renewal of the stem compartment by these cells. Here we demonstrate that β3-AR blockade in the TME by inducing the differentiation of different stromal cells at the expense of stemness traits could possibly have a favorable effect on the control of melanoma progression.

show abstract

Section: Discussionmentioning

confidence: 99%

β3-Adrenoreceptor Blockade Induces Stem Cells Differentiation in Melanoma Microenvironment

Calvani

Bruno

Dabraio

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…CSCs (“seeds”) reside in and are regulated by niches (“soil”) composed of an extracellular matrix, and differentiated and stromal cells, such as fibroblasts, vascular endothelial and inflammatory cells, and mesenchymal and hematopoietic stem cells. 7 These cells produced factors that trigger multiple signaling pathways in CSCs to promote self-renewal, invasion, metastasis, and tumorigenicity. 8 , 9 In addition, niches induced differentiated cancer cells subsequently to dedifferentiate into CSCs, 8 and niches sheltered CSCs from xenobiotics, X-rays, and ions, which explains CSC resistance to chemotherapy and conventional radiotherapy.…”

Section: Introductionmentioning

confidence: 99%

“… 8 , 9 In addition, niches induced differentiated cancer cells subsequently to dedifferentiate into CSCs, 8 and niches sheltered CSCs from xenobiotics, X-rays, and ions, which explains CSC resistance to chemotherapy and conventional radiotherapy. 7 …”

Section: Introductionmentioning

confidence: 99%

Monitoring cancer stem cells: insights into clinical oncology

Lin

Gan

et al. 2016

OTT

Self Cite

View full text Add to dashboard Cite

Cancer stem cells (CSCs) are a small, characteristically distinctive subset of tumor cells responsible for tumor initiation and progression. Several treatment modalities, such as surgery, glycolytic inhibition, driving CSC proliferation, immunotherapy, and hypofractionated radiotherapy, may have the potential to eradicate CSCs. We propose that monitoring CSCs is important in clinical oncology as CSC populations may reflect true treatment response and assist with managing treatment strategies, such as defining optimal chemotherapy cycles, permitting pretreatment cancer surveillance, conducting a comprehensive treatment plan, modifying radiation treatment, and deploying rechallenge chemotherapy. Then, we describe methods for monitoring CSCs.

show abstract

Effects of Recombinant Adenovirus-Mediated Co-Transfection of CEA Gene and EPO Geneon Promoting Hematopoietic Stem Cell Directly Producing Erythrocyte Vaccine against Colon Cancer

孙¹

2018

HJS

View full text Add to dashboard Cite

Objective: To investigate the effects of recombinant adenovirus-mediated co-transfection of CEA gene and EPO gene on promoting hematopoietic stem cell directly producing erythrocyte vaccine against colon cancer. Method: The expression adenovirus vectors carrying CEA and EPO or green fluorescent protein (GFP) gene were constructed respectively, and recombinant adenovirus carrying CEA, EPO or GFP were packaged and produced respectively. The bone marrow-derived MSCs of mice were isolated and cultured in vitro by anti-CD117magnetic bead separation, and were transfected with CEA (CEA group), EPO (EPO group) or GFP(GFP group), co-transfected with CEA and EPO (CEA and EPO group), or transfected with no virus (controlgroup). The expression of CEA and EPO gene and protein after transfection in supernatant fluid of culture was detected by RT-PCR and western blot in each group. We have checked and obtained the vaccine with co-transfection of CEA gene and EPO gene by cell red line marker antibody CD71 and GPA, then we carried on experiments with the vaccine in vitro and in vivo. Result: We have successfully gathered the hematopoietic stem cells; flow cytometry analysis result showed that there were significant differences before and after purification (P < 0.05). The expression of double genes (CEA-EPO gene) and protein shows CEA-EPO gene were successfully transfected into the hematopoietic stem cells. We have confirmed erythrocyte vaccine with co-transfection of CEA and EPO gene by antibody CD71 and GPA with flow cytometry. The monocytes cytotoxicity on colon cancer cell line CT26 showed that CEA-EPO group was 57.34 ± 1.13% in proportion of 40:1. Compared with CEAg group and EPO group, there was significant difference between them (P < 0.05). In the experimentation of neoplasma format, the size of murine growth of tumor was 0.29 ± 0.11 cm 3 differently in the group of CEA-EPO group; the number of murine live time on day was 69 ± 6.91 days. Compared with the group of CEA and plasmid, EPO, the group of CEA-EPO was significant differences in size and live time (P < 0.05). Conclusion: The erythrocyte vaccine with co-transfection of CEA gene and EPO gene has efficient anti-tumor effects on colon cancer. It not only can promote hematopoietic

show abstract

The correlation of hematopoietic stem cells with cancer stem cells through the regulation of stromal cells in tumor microenvironment

Cited by 3 publications

References 38 publications

β3-Adrenoreceptor Blockade Induces Stem Cells Differentiation in Melanoma Microenvironment

β3-Adrenoreceptor Blockade Induces Stem Cells Differentiation in Melanoma Microenvironment

Monitoring cancer stem cells: insights into clinical oncology

Effects of Recombinant Adenovirus-Mediated Co-Transfection of CEA Gene and EPO Geneon Promoting Hematopoietic Stem Cell Directly Producing Erythrocyte Vaccine against Colon Cancer

Contact Info

Product

Resources

About