Background and objectives: Docetaxel is a chemotherapeutic agent commonly used for treatment of many cancers, including esophageal squamous cell carcinoma. Docetaxel induces G2/M phase cell cycle arrest and ultimately cell death. In this study, we aimed to assess the effects of docetaxel on YM1 cells considering exposure time and dose.Methods: After calculating the doubling time of YM1 cells, the anti-proliferative effect of different concentrations of docetaxel (0.1-10 nM) after 24, 48 and 72 hours was assessed by the standard colorimetric assay. In addition, the effect of docetaxel on cell cycle was evaluated by flow cytometry.Results: The results showed that docetaxel toxicity was not significant until 24 hours at the tested concentrations (P>0.05). In addition, the effect of docetaxel on the cells was time-dependent at all tested concentrations. Overall, the duration of exposure to docetaxel had more significant role in docetaxel toxicity in YM1 cells compared to concentration.
Conclusion:Our findings suggest that the cytotoxicity of docetaxel on YM1 cells is time-dependent.
Background: SOX2OT is a novel cancer associated long non-coding RNA (LncRNA) with higher expression in variable tumor tissues, including esophageal squamous cell carcinoma (ESCC). It also plays an important function in embryonic neuronal development. Regarding its function in both stemness and carcinogenesis, here, we aimed to investigate its expression and function in tumorspheres of the esophagus using the RNAi method. Material & Methods: Two esophageal squamous cancer cells (ESCC): KYSE30 and YM1 cells were used for sphere enrichment. Cells were transfected with SOX2OT targeting and control siRNA. The size and the number of spheres were measured using light microscopy. Gene expression of the pluripotency genes was measured by qRT-PCR and docetaxel chemoresistance was assessed by MTS viability assay. Results: Our findings showed that ESCC tumorspheres overexpress SOX2OT gene along with other stemness genes (SOX2, OCT4A, and Nanog) compared to their original cancer cells. RNAi experiments indicated that SOX2OT knockdown can suppress the stemness-related gene expression, sphere formation ability (both size and number), and docetaxel resistance as three of the main cancer stem cell characteristics of tumorspheres. Conclusion: Altogether our results showed the regulatory role of SOX2OT in pluripotency and stemness in ESCC tumorspheres. Our results suggest a potential application of SOX2OT inhibition in combination with docetaxel for ESCC inhibition in vitro.
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