Related Experiment Video
Updated: Dec 26, 2025
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Selective Inhibition of Esophageal Cancer Stem-like Cells with Salinomycin
Mahdi Zarei1, Marie S Jazi2,3, Mahboubeh Tajaldini4
1Student Research Committee, Golestan University of Medical Sciences, Gorgan, Iran
Background:
Targeting Cancer Stem-Like Cells (CSLCs) can provide promising new therapeutic strategies to inhibit cancer progression, metastasis and recurrence. Salinomycin (Sal), an antibacterial ionophore, has been shown to inhibit CSCs specifically. Recently, it has been reported that Sal can destabilize TAZ, the hypo pathway transducer in CSLCs.
Objectives:
Here, in the current study, we aimed to assess the differential toxicity of Sal in esophageal CSLCs and its relation to TAZ gene expression.
Methods:
The esophageal cancer cell line, KYSE-30, was used for the enrichment of CSLCs. The expression of TAZ was knocked down using specific siRNA transfection and then the cytotoxicity of Sal was measured using XTT assay. The qRT-PCR method was used for gene expression assessment and the sphere formation ability was monitored using light microscopy.
Results:
Our findings showed that esophageal CSLCs over-express stemness-associated genes, including SOX2, OCT4 as well as TAZ (~14 fold, P value=0.02) transcription coactivator. We found Sal can selectively inhibit KYSE-30 CSLCs viability and sphere formation ability; however, TAZ knockdown does not change its differential toxicity.
Conclusion:
Overall, our results indicated that Sal can selectively decrease the viability of esophageal CSLCs in a TAZ-independent manner.
Insights
Salinomycin selectively inhibits esophageal cancer stem-like cells (CSLCs) viability. This effect is independent of TAZ gene expression, a key pathway transducer in CSLCs, suggesting a novel therapeutic approach.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Stem Cell Research
Background:
- Targeting cancer stem-like cells (CSLCs) offers therapeutic strategies against cancer progression, metastasis, and recurrence.
- Salinomycin (Sal), an ionophore, specifically inhibits CSLCs and has been reported to destabilize TAZ, a key transducer in CSLCs.
Purpose of the Study:
- To assess the differential toxicity of Salinomycin in esophageal CSLCs.
- To investigate the relationship between Salinomycin's toxicity and TAZ gene expression in esophageal CSLCs.
Main Methods:
- Enrichment of CSLCs from the KYSE-30 esophageal cancer cell line.
- TAZ gene knockdown using siRNA, followed by Salinomycin cytotoxicity assessment via XTT assay.
- Gene expression analysis using qRT-PCR and monitoring of sphere formation ability.
Main Results:
- Esophageal CSLCs over-expressed stemness genes SOX2, OCT4, and TAZ (approximately 14-fold increase, P=0.02).
- Salinomycin selectively inhibited the viability and sphere formation of KYSE-30 CSLCs.
- TAZ knockdown did not alter the differential toxicity of Salinomycin.
Conclusions:
- Salinomycin selectively reduces the viability of esophageal CSLCs.
- The anti-CSLC effect of Salinomycin is independent of TAZ expression.
