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Published on: May 21, 2019
MicroRNA-203 inhibits cell proliferation by repressing ΔNp63 expression in human esophageal squamous cell carcinoma
Yang Yuan1, Zhi-Yong Zeng, Xiao-Hong Liu
1Institute of Cardiothoracic Surgery, Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, PR China.
Background:
This study was performed to investigate the effect of microRNA-203 (miR-203) and ΔNp63 on cell proliferation and the functional connection between miR-203 and ΔNp63 in ESCC.
Methods:
We employed 2 human ESCC cell lines, Eca109 and TE-1, as the model system. The effect of miR-203 and ΔNp63 on cell proliferation was determined in cells transfected with miR-203 mimic and ΔNp63 small interfering RNA (siRNA), respectively. The regulation of ΔNp63 expression in ESCC cells by miR-203 was studied by luciferase reporter assay, RT-PCR and western blot analysis in cells transfected with miR-203. The effect of ΔNp63 re-expression on miR-203 induced inhibition of cell proliferation was studied by cell proliferation assay in cells cotransfected with miR-203 and pcDNA-ΔNp63 plasmid (without the 3'-UTR of ΔNp63).
Results:
We found that both miR-203 and ΔNp63 siRNA signicantly inhibited cell proliferation in ESCC. MiR-203 could down-regulate endogenous ΔNp63 expression at the posttranscriptional level. Moreover, re-expression of ΔNp63 in cells transfected with miR-203 significantly attenuated the miR-203 induced inhibition of cell proliferation.
Conclusions:
Our data implied that miR-203 could inhibit cell proliferation in human ESCC through ΔNp63-mediated signal pathway. Therefore, we propose that miR-203 might be used as a therapeutic agent for human ESCC.
Insights
MicroRNA-203 (miR-203) inhibits esophageal squamous cell carcinoma (ESCC) cell proliferation by downregulating ΔNp63. This suggests miR-203 may serve as a potential therapeutic agent for ESCC treatment.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- Esophageal squamous cell carcinoma (ESCC) is a significant global health concern.
- The roles of microRNA-203 (miR-203) and ΔNp63 in ESCC progression are not fully understood.
- Investigating the interplay between miR-203 and ΔNp63 is crucial for understanding ESCC pathogenesis.
Purpose of the Study:
- To investigate the effect of miR-203 and ΔNp63 on cell proliferation in ESCC.
- To elucidate the functional connection between miR-203 and ΔNp63 in ESCC.
- To explore the potential of miR-203 as a therapeutic agent for ESCC.
Main Methods:
- Utilized human ESCC cell lines (Eca109, TE-1).
- Assessed cell proliferation following transfection with miR-203 mimic or ΔNp63 siRNA.
- Examined miR-203 regulation of ΔNp63 using luciferase reporter assays, RT-PCR, and Western blot.
- Investigated the impact of ΔNp63 re-expression on miR-203's anti-proliferative effects.
Main Results:
- Both miR-203 and ΔNp63 siRNA significantly inhibited ESCC cell proliferation.
- miR-203 was found to down-regulate endogenous ΔNp63 expression post-transcriptionally.
- Re-expression of ΔNp63 attenuated the miR-203-induced inhibition of cell proliferation.
Conclusions:
- miR-203 inhibits cell proliferation in human ESCC via a ΔNp63-mediated signaling pathway.
- The findings suggest that miR-203 holds potential as a therapeutic agent for human ESCC.
- Targeting the miR-203/ΔNp63 axis could be a promising strategy for ESCC treatment.
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