Cancer stem cells and differentiation therapy

Jin, Xiong; Jin, Xun; Kim, Hyunggee

doi:10.1177/1010428317729933

Cited by 86 publications

(71 citation statements)

References 161 publications

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“…Once the regulatory balance is destroyed, uncontrolled CSCs ultimately lead to tumorigenesis. 21 CSCs also transdifferentiate into other multilineage cells to regulate tumorigenesis. 22 Bussolati et al 23 found that renal CSCs differentiated into vascular endothelial cells (ECs) in the bulk of tumors formed in SCID mice after injection of human renal CSCs.…”

Section: The Concept Of Cscs Biological Characteristics Of Cscsmentioning

confidence: 99%

Targeting cancer stem cell pathways for cancer therapy

Yang

Shi

Zhao

et al. 2020

Sig Transduct Target Ther

1,225

998

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Since cancer stem cells (CSCs) were first identified in leukemia in 1994, they have been considered promising therapeutic targets for cancer therapy. These cells have self-renewal capacity and differentiation potential and contribute to multiple tumor malignancies, such as recurrence, metastasis, heterogeneity, multidrug resistance, and radiation resistance. The biological activities of CSCs are regulated by several pluripotent transcription factors, such as OCT4, Sox2, Nanog, KLF4, and MYC. In addition, many intracellular signaling pathways, such as Wnt, NF-κB (nuclear factor-κB), Notch, Hedgehog, JAK-STAT (Janus kinase/signal transducers and activators of transcription), PI3K/AKT/mTOR (phosphoinositide 3-kinase/AKT/mammalian target of rapamycin), TGF (transforming growth factor)/SMAD, and PPAR (peroxisome proliferator-activated receptor), as well as extracellular factors, such as vascular niches, hypoxia, tumor-associated macrophages, cancer-associated fibroblasts, cancer-associated mesenchymal stem cells, extracellular matrix, and exosomes, have been shown to be very important regulators of CSCs. Molecules, vaccines, antibodies, and CAR-T (chimeric antigen receptor T cell) cells have been developed to specifically target CSCs, and some of these factors are already undergoing clinical trials. This review summarizes the characterization and identification of CSCs, depicts major factors and pathways that regulate CSC development, and discusses potential targeted therapy for CSCs.Signal Transduction and Targeted Therapy (2020) 5:8; https://doi.

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Section: The Concept Of Cscs Biological Characteristics Of Cscsmentioning

confidence: 99%

Targeting cancer stem cell pathways for cancer therapy

Yang

Shi

Zhao

et al. 2020

Sig Transduct Target Ther

1,225

998

View full text Add to dashboard Cite

show abstract

“…Specific gene expression profiles are needed for tumor cell differentiation which are dictated through different signaling pathways, transcription factor activities, as well as epigenetic alterations such as DNA modifications (Jögi, Vaapil, Johansson, & Påhlman, 2012). The involved signaling pathways in CSCs differentiation are BMP (bone morphogenetic protein) and RA (retinoic acid) pathways, while CSCs stemness signaling cascades include JAK/ STAT, Wnt/β-catenin, Hedgehog, Notch, PI3K/PTEN, and NF-kB (Jin et al, 2017;Matsui, 2016). The expression profile of differentiation-associated genes is heterogeneous in nearly all types of tumor cells, probably due to the transcriptional activity of a small population of CSCs in combination with numerous partially differentiated cells (Palmer, Schmid, Berger, & Kohane, 2012).…”

Section: Introductionmentioning

confidence: 99%

“…The expression profile of differentiation-associated genes is heterogeneous in nearly all types of tumor cells, probably due to the transcriptional activity of a small population of CSCs in combination with numerous partially differentiated cells (Palmer, Schmid, Berger, & Kohane, 2012). Inhibition of differentiation happens through highly expressed ID (Inhibitor of DNA-binding/ differentiation) proteins as regulators of cell fate (Jin et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

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MEIS1 knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE‐30

Mahmoudian

Bahadori

Rad

et al. 2019

Molec Gen & Gen Med

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Background MEIS1 (Myeloid ecotropic viral integration site 1), as a homeobox (HOX) transcription factor, has a dual function in different types of cancer. Although numerous roles are proposed for MEIS1 in differentiation, stem cell function, gastrointestinal development and tumorigenesis, the involved molecular mechanisms are poor understood. Our aim in this study was to elucidate the functional correlation between MEIS1 , as regulator of differentiation process, and the involved genes in cell differentiation in human esophageal squamous carcinoma (ESC) cell line KYSE‐30. Methods The KYSE‐30 cells were transduced using recombinant retroviral particles containing specific shRNA sequence against MEIS1 to knockdown MEIS1 gene expression. Following RNA extraction and cDNA synthesis, mRNA expression of MEIS1 and the selected genes including TWIST1, EGF, CDX2, and KRT4 was examined using relative comparative real‐time PCR. Results Retroviral transduction caused a significant underexpression of MEIS1 in GFP‐hMEIS1 compared to control GFP cells approximately 5.5‐fold. While knockdown of MEIS1 expression caused a significant decrease in EGF and TWIST1 mRNA expression, nearly ‐8‐ and ‐12‐fold respectively, it caused a significant increase in mRNA expression of differentiation markers including KRT4 and CDX2 , approximately 34‐ and 1.14‐fold, correspondingly. Conclusion MEIS1 gene silencing in KYSE‐30 cells increased expression of epithelial markers and decreased expression of epithelial‐mesenchymal transition (EMT) marker TWIST1 . It may highlight the role of MEIS1 in differentiation process of KYSE‐30 cells. These results may confirm that MEIS1 silencing promotes differentiation and decreases EMT capability of ESC cell line KYSE‐30.

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“…(all-trans-retinoic acid) and its analogs, HDACI, miR-100, tyrosine kinase, and signal pathways inhibitors can induce CSCs into differentiated cancer cells which could be treated with anti-cancer agents. In addition, to increase sensitivity to cancer treatment, differentiation of CSCs can decrease motility and tumorigenicity of CSCs, and reduce invasion and migration of tumor [41][42][43][44].…”

Section: Induction Of Cscs Differentiation By Agents Like Atramentioning

confidence: 99%

Cancer stem cells as therapeutic targets of pancreatic cancer

Razi

Radak

Mahjoubin‐Tehran

et al. 2019

Fundamemntal Clinical Pharma

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The discovery of stem cells and their potential abilities in self‐renewal and differentiation has opened a new horizon in medicine. Scientists have found a small population of stem cells in some types of cancers with the same functions as normal stem cells. There are two models for tumor progression: clonal (stochastic) and cancer stem cell (CSCs) models. According to the first model, all transformed cells in the tumor have carcinogenic potential and are able to proliferate and produce the same cells. The latter model, which has received more attention recently, considers the role of CSCs in drug resistance and tumor metastasis. Following the model, researchers have found that targeting CSCs may be a promising way in cancer therapy. This review describes CSC characteristics in general, while also focusing on CSC properties in the context of pancreatic cancer.

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Cancer stem cells and differentiation therapy

Cited by 86 publications

References 161 publications

Targeting cancer stem cell pathways for cancer therapy

Targeting cancer stem cell pathways for cancer therapy

MEIS1 knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE‐30

Cancer stem cells as therapeutic targets of pancreatic cancer

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