Cytokines, breast cancer stem cells (BCSCs) and chemoresistance

Chen, Weilong; Qin, Yuanyuan; Liu, Suling

doi:10.1186/s40169-018-0205-6

Cited by 72 publications

(67 citation statements)

References 127 publications

(141 reference statements)

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“…Those strategies have proven to be valid and they limit tumor progression, in addition to the reduction of tumor size [29,30]. New cells that arise from CSCs could drive tumor phenotype, survival, and growth [31,32]. Here, we describe that CSCs could give non-adherent cells with a phenotype common to hematopoietic cells.…”

Section: Discussionmentioning

confidence: 91%

Hematopoietic Cells Derived from Cancer Stem Cells Generated from Mouse Induced Pluripotent Stem Cells

Hassan

Afify

Nair

et al. 2019

Cancers

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Cancer stem cells (CSCs) represent the subpopulation of cancer cells with the ability to differentiate into other cell phenotypes and initiated tumorigenesis. Previously, we reported generating CSCs from mouse induced pluripotent stem cells (miPSCs). Here, we investigated the ability of the CSCs to differentiate into hematopoietic cells. First, the primary cells were isolated from malignant tumors that were formed by the CSCs. Non-adherent cells (NACs) that arose from adherent cells were collected and their viability, as well as the morphology and expression of hematopoietic cell markers, were analyzed. Moreover, NACs were injected into the tail vein of busulfan conditioned Balb/c nude mice. Finally, CSCs were induced to differentiate to macrophages while using IL3 and SCF. The round nucleated NACs were found to be viable, positive for hematopoietic lineage markers and CD34, and expressed hematopoietic markers, just like homing to the bone marrow. When NACs were injected into mice, Wright-Giemsa staining showed that the number of white blood cells got higher than those in the control mice after four weeks. CSCs also showed the ability to differentiate toward macrophages. CSCs were demonstrated to have the potential to provide progenies with hematopoietic markers, morphology, and homing ability to the bone marrow, which could give new insight into the tumor microenvironment according to the plasticity of CSCs.

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Section: Discussionmentioning

confidence: 91%

Hematopoietic Cells Derived from Cancer Stem Cells Generated from Mouse Induced Pluripotent Stem Cells

Hassan

Afify

Nair

et al. 2019

Cancers

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“…In this sense, many attempts have been made to find the connection between drug resistance and immune evasion (89), and common pathways controlling both processes have been explored. Within the WNT signaling pathways, many molecules have been described as being the main drivers of the transcriptional activation of the genes involved in the two mechanisms (90)(91)(92)(93)(94).…”

Section: Wnt Signaling Activation In Healthy Immune Response and In Tmentioning

confidence: 99%

WNT Signaling in Tumors: The Way to Evade Drugs and Immunity

et al. 2019

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WNT/β-catenin signaling is involved in many physiological processes. Its implication in embryonic development, cell migration, and polarization has been shown. Nevertheless, alterations in this signaling have also been related with pathological events such as sustaining and proliferating the cancer stem cell (CSC) subset present in the tumor bulk. Related with this, WNT signaling has been associated with the maintenance, expansion, and epithelial-mesenchymal transition of stem cells, and furthermore with two distinctive features of this tumor population: therapeutic resistance (MDR, multidrug resistance) and immune escape. These mechanisms are developed and maintained by WNT activation through the transcriptional control of the genes involved in such processes. This review focuses on the description of the best known WNT pathways and the molecules involved in them. Special attention is given to the WNT cascade proteins deregulated in tumors, which have a decisive role in tumor survival. Some of these proteins function as extrusion pumps that, in the course of chemotherapy, expel the drugs from the cells; others help the tumoral cells hide from the immune effector mechanisms. Among the WNT targets involved in drug resistance, the drug extrusion pump MDR-1 (P-GP, ABCB1) and the cell adhesion molecules from the CD44 family are highlighted. The chemokine CCL4 and the immune checkpoint proteins CD47 and PD-L1 are included in the list of WNT target molecules with a role in immunity escape. This pathway should be a main target in cancer therapy as WNT signaling activation is essential for tumor progression and survival, even in the presence of the anti-tumoral immune response and/or antineoplastic drugs. The appropriate design and combination of anti-tumoral strategies, based on the modulation of WNT mediators and/or protein targets, could negatively affect the growth of tumoral cells, improving the efficacy of these types of therapies.

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“…Not only does this dynamic process of transformation alter the cancer cell itself, but transforming cells have a substantial impact on the surrounding environment. Evidence suggests that the accumulation of mutations within epithelial cells can lead to a dysregulated secretory network, including a number of inflammatory cytokines linked to poor prognosis, therapy failure, and disease recurrence (IL-6, IL-8, TGF-β, CCL2, TNF-α, IL-17 and others) [54][55][56][57][58][59] . This dysregulated secretory network in turn, changes the cellular composition of the TME, leading to a reciprocal cross-talk between non-cancerous stromal cells and the transforming epithelial cells.…”

mentioning

confidence: 99%

Cellular plasticity and metastasis in breast cancer: a pre- and post-malignant problem

Smigiel

Taylor

Bryson

et al. 2019

JCMT

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As a field we have made tremendous strides in treating breast cancer, with a decline in the past 30 years of overall breast cancer mortality. However, this progress is met with little affect once the disease spreads beyond the primary site. With a 5-year survival rate of 22%, 10-year of 13%, for those patients with metastatic breast cancer (mBC), our ability to effectively treat wide spread disease is minimal. A major contributing factor to this ineffectiveness is the complex make-up, or heterogeneity, of the primary site. Within a primary tumor, secreted factors, malignant and pre-malignant epithelial cells, immune cells, stromal fibroblasts and many others all reside alongside each other creating a dynamic environment contributing to metastasis. Furthermore, heterogeneity contributes to our lack of understanding regarding the cells' remarkable ability to undergo epithelial/non-cancer stem cell (CSC) to mesenchymal/CSC (E-M/CSC) plasticity. The enhanced invasion & motility, tumor-initiating potential, and acquired therapeutic resistance which accompanies E-M/CSC plasticity implicates a significant role in metastasis. While most work trying to understand E-M/CSC plasticity has been done on malignant cells, recent evidence is emerging concerning the ability for pre-malignant cells to undergo E-M/CSC plasticity and contribute to the metastatic process. Here we will discuss the importance of E-M/CSC plasticity within malignant and pre-malignant populations of the tumor. Moreover, we will discuss how one may potentially target these populations, ultimately disrupting the metastatic cascade and increasing patient survival for those with mBC.

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Cytokines, breast cancer stem cells (BCSCs) and chemoresistance

Cited by 72 publications

References 127 publications

Hematopoietic Cells Derived from Cancer Stem Cells Generated from Mouse Induced Pluripotent Stem Cells

Hematopoietic Cells Derived from Cancer Stem Cells Generated from Mouse Induced Pluripotent Stem Cells

WNT Signaling in Tumors: The Way to Evade Drugs and Immunity

Cellular plasticity and metastasis in breast cancer: a pre- and post-malignant problem

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