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
Conclusion: Overall, our results indicated that Sal can selectively decrease the viability of esophageal CSLCs in
a TAZ-independent manner.