NSPc1 promotes cancer stem cell self-renewal by repressing the synthesis of all-trans retinoic acid via targeting RDH16 in malignant glioma

Oncogene ◽  
2017 ◽  
Vol 36 (33) ◽  
pp. 4706-4718 ◽  
Author(s):  
P-S Hu ◽  
Q-S Xia ◽  
F Wu ◽  
D-k Li ◽  
Y-j Qi ◽  
...  
Keyword(s):  
Stem Cell ◽  
Retinoic Acid ◽  
Cancer Stem Cell ◽  
Malignant Glioma ◽  
Self Renewal ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

scholarly journals All-trans retinoic acid reduces cancer stem cell-like cell-mediated resistance to gefitinib in NSCLC adenocarcinoma cells

2019 ◽  
Author(s):  
Wenxiu Yao ◽  
Liyang Wang ◽  
Huan Huang ◽  
Xin Li ◽  
Pinjia Wang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Retinoic Acid ◽  
Cancer Stem Cell ◽  
Kinase Inhibitors ◽  
Small Cell ◽  
Small Cell Lung ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Egfr Tyrosine Kinase Inhibitors ◽  
Ic50 Values

Abstract Background: The enrichment of cancer stem cell-like cells (CSCs) has been considered to be responsible for tumor progression after an initial response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs) in patients with non-small cell lung adenocarcinoma (NSCLC/ADC). All-trans retinoic acid (ATRA) has been shown to potentiate cancer chemotherapy due to its ability to induce signals for CSC differentiation. We therefore investigated whether ATRA could improve the response of NSCLC/ADC cells to TKI gefitinib. Methods: Treatment of NSCLC/ADC A549 and H1650 cells with gefitinib enriched the gefitinib surviving cells (GSCs). The expression of ALDH1A1 and CD44 and the IC50 values for gefitinib were determined by flow cytometry (FCM) and crystal violet assay in GSCs and ATRA-treated GSCs, respectively. Results: GSCs showed higher expression of ALDH1A1 and CD44 and IC50 values for gefitinib than their respective parental cells, suggesting that gefitinib can lead to propagation of CSC-enriched gefitinib-resistant cells. Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells. Conclusion: Our findings suggest that combination treatment with ATRA prevents gefitinib-induced enrichment of ALDH1A1bright/CD44high CSCs and enhances gefitinib-induced growth inhibition of NSCLC/ADC cells. Key words: All-trans retinoic acid, ALDH1A1, CD44, EGFR tyrosine kinase inhibitors, non-small cell lung adenocarcinoma

scholarly journals All-trans retinoic acid reduces cancer stem cell-like cell-mediated resistance to gefitinib in NSCLC adenocarcinoma cells

2020 ◽  
Author(s):  
Wenxiu Yao ◽  
Liyang Wang ◽  
Huan Huang ◽  
Xin Li ◽  
Pinjia Wang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Retinoic Acid ◽  
Cancer Stem Cell ◽  
Kinase Inhibitors ◽  
Growth Factor Receptor ◽  
Initial Response ◽  
Inhibitory Effect ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Ic50 Values

Abstract Background: The enrichment of cancer stem cell-like cells (CSCs) has been considered to be responsible for tumor progression after an initial response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs) in patients with non-small cell lung adenocarcinoma (NSCLC/ADC). CSCs with ALDH1A1bright /CD44high expression contribute to the TKIs resistance in NSCLC/ADC cells. All-trans retinoic acid (ATRA) has been shown to be a potential targeted therapy against CSCs due to its ability to inhibit ALDH1A1 activity. We therefore investigated whether ATRA could circumvent the resistance to improve the response to gefitinib in NSCLC/ADC cells.Methods: Treatment of NSCLC/ADC A549 and H1650 cells with gefitinib enriched the gefitinib surviving cells (GSCs). The expression of ALDH1A1 and CD44 and the IC50 values for gefitinib were determined by flow cytometry (FCM) and crystal violet assay in GSCs and ATRA-treated GSCs, respectively. Using DEAB as the positive control, direct inhibitory effect of ATRA on ALDH1A1 activity was determined by ALDEFLUOR assay, Results: GSCs showed higher expression of ALDH1A1 and CD44 and IC50 values for gefitinib than their respective parental cells, suggesting that gefitinib can lead to propagation of CSC-enriched gefitinib-resistant cells. Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells, and ATRA could directly inhibit active ALDH1A1 as compared to DEAB.Conclusion: Our findings suggest that combination treatment with ATRA prevents gefitinib-induced enrichment of ALDH1A1bright/CD44high CSCs and enhances gefitinib-induced growth inhibition of NSCLC/ADC cells.

scholarly journals All-trans retinoic acid reduces cancer stem cell-like cell-mediated resistance to gefitinib in NSCLC adenocarcinoma cells

2020 ◽  
Author(s):  
Wenxiu Yao ◽  
Liyang Wang ◽  
Huan Huang ◽  
Xin Li ◽  
Pinjia Wang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Retinoic Acid ◽  
Cancer Stem Cell ◽  
Kinase Inhibitors ◽  
Small Cell ◽  
Small Cell Lung ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Egfr Tyrosine Kinase Inhibitors ◽  
Ic50 Values

Abstract Background: The enrichment of cancer stem cell-like cells (CSCs) has been considered to be responsible for tumor progression after an initial response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs) in patients with non-small cell lung adenocarcinoma (NSCLC/ADC). CSCs with ALDH1A1 bright /CD44 high expression contribute to the TKIs resistance in NSCLC/ADC cells. All-trans retinoic acid (ATRA) has been shown to be a potential targeted therapy against CSCs due to its ability to inhibit ALDH1A1 activity. We therefore investigated whether ATRA could circumvent the resistance to improve the response to gefitinib in NSCLC/ADC cells. Methods: Treatment of NSCLC/ADC A549 and H1650 cells with gefitinib enriched the gefitinib surviving cells (GSCs). The expression of ALDH1A1 and CD44 and the IC50 values for gefitinib were determined by flow cytometry ( FCM ) and crystal violet assay in GSCs and ATRA-treated GSCs, respectively. Using DEAB as the positive control, direct inhibitory effect of ATRA on ALDH1A1 activity was determined by ALDEFLUOR assay. Results: GSCs showed higher expression of ALDH1A1 and CD44 and IC50 values for gefitinib than their respective parental cells, suggesting that gefitinib can lead to propagation of CSC-enriched gefitinib-resistant cells. Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells, and ATRA could directly inhibit active ALDH1A1 as compared to DEAB. Conclusion: Our findings suggest that combination treatment with ATRA prevents gefitinib-induced enrichment of ALDH1A1 bright /CD44 high CSCs and enhances gefitinib-induced growth inhibition of NSCLC/ADC cells. Key words : All-trans retinoic acid, ALDH1A1, CD44, EGFR tyrosine kinase inhibitors, non-small cell lung adenocarcinoma

scholarly journals All-trans retinoic acid reduces cancer stem cell-like cell-mediated resistance to gefitinib in NSCLC adenocarcinoma cells

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Wenxiu Yao ◽  
Liyang Wang ◽  
Huan Huang ◽  
Xin Li ◽  
Pinjia Wang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Retinoic Acid ◽  
Cancer Stem Cell ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Adenocarcinoma Cells

scholarly journals All-trans retinoic acid reduces cancer stem cell-like cell-mediated resistance to gefitinib in NSCLC adenocarcinoma cells

2020 ◽  
Author(s):  
Wenxiu Yao ◽  
Liyang Wang ◽  
Huan Huang ◽  
Xin Li ◽  
Pinjia Wang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Retinoic Acid ◽  
Cancer Stem Cell ◽  
Kinase Inhibitors ◽  
Small Cell ◽  
Small Cell Lung ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Egfr Tyrosine Kinase Inhibitors ◽  
Ic50 Values

Abstract Background: The enrichment of cancer stem cell-like cells (CSCs) has been considered to be responsible for tumor progression after an initial response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs) in patients with non-small cell lung adenocarcinoma (NSCLC/ADC). CSCs with ALDH1A1 bright /CD44 high expression contribute to the TKIs resistance in NSCLC/ADC cells. All-trans retinoic acid (ATRA) has been shown to be a potential targeted therapy against CSCs due to its ability to inhibit ALDH1A1 activity. We therefore investigated whether ATRA could circumvent the resistance to improve the response to gefitinib in NSCLC/ADC cells. Methods: Treatment of NSCLC/ADC A549 and H1650 cells with gefitinib enriched the gefitinib surviving cells (GSCs). The expression of ALDH1A1 and CD44 and the IC50 values for gefitinib were determined by flow cytometry ( FCM ) and crystal violet assay in GSCs and ATRA-treated GSCs, respectively. Using DEAB as the positive control, direct inhibitory effect of ATRA on ALDH1A1 activity was determined by ALDEFLUOR assay, Results: GSCs showed higher expression of ALDH1A1 and CD44 and IC50 values for gefitinib than their respective parental cells , suggesting that gefitinib can lead to propagation of CSC -enriched gefitinib -resistant cells. Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells, and ATRA could directly inhibit active ALDH1A1 as compared to DEAB. Conclusion: Our findings suggest that combination treatment with ATRA prevents gefitinib-induced enrichment of ALDH1A1 bright /CD44 high CSCs and enhances gefitinib-induced growth inhibition of NSCLC/ADC cells. Key words : All-trans retinoic acid, ALDH1A1, CD44, EGFR tyrosine kinase inhibitors, non-small cell lung adenocarcinoma

scholarly journals Therapeutic Use of Valproic Acid and All-Trans Retinoic Acid in Acute Myeloid Leukemia—Literature Review and Discussion of Possible Use in Relapse after Allogeneic Stem Cell Transplantation

2021 ◽  
Vol 14 (5) ◽  
pp. 423
Author(s):  
Øystein Bruserud ◽  
Galina Tsykunova ◽  
Maria Hernandez-Valladares ◽  
Hakon Reikvam ◽  
Tor Henrik Anderson Tvedt
Keyword(s):  
Valproic Acid ◽  
Acute Myeloid Leukemia ◽  
Stem Cell ◽  
Retinoic Acid ◽  
Myeloid Leukemia ◽  
Low Intensity ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Low Toxicity ◽  
Acute Myeloid

Even though allogeneic stem cell transplantation is the most intensive treatment for acute myeloid leukemia (AML), chemo-resistant leukemia relapse is still one of the most common causes of death for these patients, as is transplant-related mortality, i.e., graft versus host disease, infections, and organ damage. These relapse patients are not always candidates for additional intensive therapy or re-transplantation, and many of them have decreased quality of life and shortened expected survival. The efficiency of azacitidine for treatment of posttransplant AML relapse has been documented in several clinical trials. Valproic acid is an antiepileptic fatty acid that exerts antileukemic activity through histone deacetylase inhibition. The combination of valproic acid and all-trans retinoic acid (ATRA) is well tolerated even by unfit or elderly AML patients, and low-toxicity chemotherapy (e.g., azacitidine) can be added to this combination. The triple combination of azacitidine, valproic acid, and ATRA may therefore represent a low-intensity and low-toxicity alternative for these patients. In the present review, we review and discuss the general experience with valproic acid/ATRA in AML therapy and we discuss its possible use in low-intensity/toxicity treatment of post-allotransplant AML relapse. Our discussion is further illustrated by four case reports where combined treatments with sequential azacitidine/hydroxyurea, valproic acid, and ATRA were used.

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