Concise Reviews: Cancer Stem Cell Targeted Therapies: Toward Clinical Success

Desai, Amar; Yan, Yan; Gerson, Stanton L.

doi:10.1002/sctm.18-0123

Cited by 149 publications

(127 citation statements)

References 76 publications

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“…It is well established that targeting CSCs reduces relapse and metastases in cancer patients. Moreover, by combining CSCs, targeted therapies with conventional one tumors could be eradicated [26]. Targeting stemness pathways and microenvironment components while using stemness markers, or immunological approaches are some examples of recent efforts for designing more effective cancer treatments [27,28].…”

Section: Discussionmentioning

confidence: 99%

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: 99%

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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“… Gefitinib (EGFR tyrosine kinase inhibitor) Inhibited EGFR signaling and reduced SOX2 expression in TSCC cells TSCC [ 213 , 214 ] 5. Combination therapy of SN-38 and gefitinib inhibits the expression of CD44 stemness marker by promoting its lysosomal degradation in TSCC cells TSCC [110] 6 GSK1120212 MEK1/2 inhibitor in TSCC TSCC [215] 7 Simvastatin & AR-42 (TAZ inhibitors) TAZ (PDZ-binding motif) inhibited tumor growth in-vivo, reduced cell proliferation, migration and tumorsphere formation in TSCC cells TSCC and TCSC [ 216 , 217 ] 8. FLI-06 (NOTCH inhibitor) Inhibited tumor growth and increased cell apoptosis, suppressed both the mRNA and protein expression of Notch receptor and block the proliferation and self-renewal of tongue cancer stem cells.…”

Section: Various Molecular Approaches/signaling Pathways For Targetinmentioning

confidence: 99%

HPV+ve/−ve oral-tongue cancer stem cells: A potential target for relapse-free therapy

Gupta

Kumar

Das

2021

Translational Oncology

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Highlights Tongue squamous cell carcinoma (TSCC) is most aggressive and highly prevalent subtype of head and neck cancer. Majority of tobacco users are HPV −ve and have bad prognosis while HPV +ve TSCCs not using tobacco show better prognosis. Tongue cancer stem cells (TCSCs) are resistant to chemo-radio therapy and responsible for cancer relapse. Targeting TCSCs may provide efficient therapeutic strategy for relapse-free survival of TSCC patients.

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“…1C). One of the critical properties of CSCs is their potential to differentiate into unlimited heterogeneous populations of cancer cells (Desai et al, 2018). To investigate the differentiation potential of the long-term sorafenib-treated cells, HepG2, Huh7, HepG2SF1 and Huh7SF1 cells were incubated in neuronal differentiation or glial differentiation media for 15 days.…”

Section: Sorafenib Resistance In Hcc Cells Induces a Stem-like Phenotypementioning

confidence: 99%

Targeting AMP‐activated kinase impacts hepatocellular cancer stem cells induced by long‐term treatment with sorafenib

et al. 2019

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Hepatocellular carcinoma ( HCC ) is the third leading cause of cancer death worldwide. HCC treatment is hindered by the frequent emergence of chemoresistance to the multikinase inhibitor sorafenib, which has been related to the presence of cancer stem cells ( CSC s) that self‐renew and often escape therapy. The key metabolic sensor AMP ‐activated kinase ( AMPK ) has recently been recognized as a tumour growth regulator. In this study, we aimed to elucidate the role of AMPK in the development of a stem cell phenotype in HCC cells. To this end, we enriched the CSC population in HCC cell lines that showed increased expression of drug resistance ( ALDH 1A1, ABCB 1A) and stem cell ( CD 133, Nanog, Oct4, alpha fetoprotein) markers and demonstrated their stemness phenotype. These cells were refractory to sorafenib‐induced cell death. We report that sorafenib‐resistant cells had lower levels of total and phosphorylated AMPK as well as its downstream substrate, ACC , compared with the parental cells. Interestingly, AMPK knockdown with si RNA or inhibition with dorsomorphin increased the expression of stem cell markers in parental cells and blocked sorafenib‐induced cell death. Conversely, the upregulation of AMPK , either by transfection or by pharmacological activation with A‐769662, decreased the expression of ALDH 1A1, ABCB 1A, CD 133, Nanog, Oct4, and alpha fetoprotein, and restored sensitivity to sorafenib. Analysis of the underlying mechanism points to hypoxia‐inducible factor HIF ‐1α as a regulator of stemness. In vivo studies in a xenograft mouse model demonstrated that stem‐like cells have greater tumourigenic capacity. AMPK activation reduced xenograft tumour growth and decreased the expression of stem cell markers. Taken together, these results indicate that AMPK may serve as a novel target to overcome chemoresistance in HCC .

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Concise Reviews: Cancer Stem Cell Targeted Therapies: Toward Clinical Success

Cited by 149 publications

References 76 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

HPV+ve/−ve oral-tongue cancer stem cells: A potential target for relapse-free therapy

Targeting AMP‐activated kinase impacts hepatocellular cancer stem cells induced by long‐term treatment with sorafenib

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