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Published on: September 8, 2017
miR-194-3p represses the docetaxel resistance in colon cancer by targeting KLK10
Jinlai Zhao1, Yigang Wang2, Yang Wang1
1Department of Gastrointestinal Surgery, Tangshan Central Hospital, Tangshan 063000, China.
Background:
Docetaxel (DCT) is widely adopted in chemotherapy for colon cancer (CC). However, DCT resistance can cause chemotherapy failure in CC. MicroRNAs (miRNAs) are key regulators of DCT resistance. Among them, miR-194-3p is a key tumor suppressor, but how it regulates DCT resistance has not been reported yet. This research explored the molecular mechanism of miR-194-3p/Kallikrein Related Peptidase 10 (KLK10) axis in regulating DCT resistance in CC.
Methods:
The expression and targeting relationship of miR-194-3p and KLK10 was dug through bioinformatics analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) was adopted to determine miR-194-3p level in CC cells. The over-expressed miR-194-3p cell group was constructed to ascertain the impacts of dysregulated miR-194-3p on DCT resistance. Through dual-luciferase assay, the targeting relationship of miR-194-3p and KLK10 was uncovered. Subsequently, the in vitro cellular experiments were performed to investigate the impacts of miR-194-3p/KLK10 axis on DCT resistance in CC cells.
Results:
We noticed that miR-194-3p was notably down-regulated in CC cells. The over-expressed miR-194-3p restored the DCT sensitivity of SW620/DCT and SW480/DCT cells. Dual-luciferase assay suggested the targeting relationship of miR-194-3p and KLK10. Besides, miR-194-3p negatively regulated KLK10 expression level. In vitro cellular experiments further exposed that miR-194-3p could down-regulate KLK10, thereby attenuating DCT resistance in CC cells.
Significance:
miR-194-3p could overcome DCT resistance in CC cells through negatively regulating KLK10. This finding offers a potential therapeutic target for clinical treatment of DCT chemoresistance in CC.
Insights
MicroRNA-194-3p overcomes docetaxel resistance in colon cancer by downregulating KLK10. This discovery offers a new therapeutic target for improving chemotherapy effectiveness in colon cancer patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Docetaxel (DCT) is a key chemotherapy for colon cancer (CC).
- Drug resistance, particularly to DCT, is a major cause of treatment failure in CC.
- MicroRNAs (miRNAs) are critical regulators of DCT resistance, with miR-194-3p identified as a potential tumor suppressor.
Purpose of the Study:
- To investigate the molecular mechanism of the miR-194-3p/Kallikrein Related Peptidase 10 (KLK10) axis in regulating DCT resistance in CC.
- To explore the potential of targeting this axis for overcoming DCT chemoresistance.
Main Methods:
- Bioinformatics analysis to identify expression and targeting relationships.
- Quantitative real-time polymerase chain reaction (qRT-PCR) to measure miR-194-3p levels.
- Dual-luciferase assay to confirm the direct targeting of KLK10 by miR-194-3p.
- In vitro cellular experiments to assess the impact of miR-194-3p/KLK10 on DCT resistance.
Main Results:
- miR-194-3p was significantly downregulated in CC cells.
- Overexpression of miR-194-3p restored sensitivity to DCT in resistant CC cell lines (SW620/DCT and SW480/DCT).
- miR-194-3p was confirmed to directly target and negatively regulate KLK10 expression.
- miR-194-3p attenuated DCT resistance in CC cells by downregulating KLK10.
Conclusions:
- miR-194-3p effectively overcomes DCT resistance in colon cancer cells by negatively regulating KLK10.
- The miR-194-3p/KLK10 pathway represents a promising therapeutic target for managing DCT chemoresistance in CC.
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