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Over-expression of miR-206 decreases the Euthyrox-resistance by targeting MAP4K3 in papillary thyroid carcinoma
Fangzhou Liu1, Rong Yin2, Xinyuan Chen3
1Department of Head & Neck Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, 210009, PR China.
Purpose:
microRNAs (miRNAs) play a critical role in drug resistance of multiple cancers including papillary thyroid carcinoma (PTC), indicating the potential of miRNAs as chemoresistance regulators in cancer treatment. The aim of this paper is to explore the relationship between miR-206 and chemoresistance of PTC.
Methods:
qRT-PCR was conducted to examine the expression of miR-206 in PTC tissues, parental and TPC-1/euthyrox. The CCK-8 assay, EdU assay and flow cytometry were performed to test cells viability, proliferation and apoptosis, respectively. Luciferase reporter assay was used to confirm the potential target of miR-206. Western blotting analysis was performed to evaluate the expressions of related-proteins.
Results:
miR-206 was significantly down-regulated in PTC tissues, parental and TPC-1/euthyrox. Moreover, the expression of miR-206 was exceptionally lower in TPC-1/euthyrox cells than that in TPC-1 cells. Furthermore, we found that over-expression of miR-206 could notably decrease the IC50 values both in TPC-1 and TPC-1/euthyrox cells, which indicated that miR-206 played an essential role in the euthyrox resistance in PTC. In addition, up-regulation of miR-206 inhibited the proliferation, induced apoptosis, suppressed the expressions of multidrug resistance-related proteins, including p-gp, MRP, BCRP and LRP, in euthyrox-resistant PTC cells. Besides, over-expression of miR-206 could notably promoted the expression of NIS, an intrinsic membrane protein that mediates the active transport of iodide into the thyroid and other tissues, playing a critical role in the progress. Further, miR-206 was demonstrated to be able to bind to MAP4K3 and negatively regulated the expression of MAP4K3. Besides, MAP4K3 was clearly up-regulated in PTC tissues, parental and TPC-1/euthyrox cells, and down-regulation of miR-206 attenuated the effect of si-MAP4K3 on the euthyrox sensitivity in euthyrox-resistant PTC cells. Moreover, TPC-1/euthyrox cells transfected with miR-206 mimics could significantly inhibit the expressions of p-p38, p-JNK and p-Erk, which indicated that miR-206 might play an essential role in the euthyrox resistance in PTC by negatively regulating the p38 and JNK signaling pathway.
Conclusion:
miR-206 contributed to euthyrox resistance in PTC cells through blockage p38 and JNK signaling pathway by targeting MAP4K3, providing a potential therapeutic application for the treatment of patients with euthyrox-resistant PTC in the further.
Insights
MicroRNA-206 (miR-206) is downregulated in papillary thyroid carcinoma (PTC) and contributes to euthyrox resistance by targeting MAP4K3 and blocking p38 and JNK signaling pathways. This finding offers potential therapeutic strategies for euthyrox-resistant PTC.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- MicroRNAs (miRNAs) are crucial in regulating drug resistance across various cancers, including papillary thyroid carcinoma (PTC).
- Understanding the role of specific miRNAs, like miR-206, in chemoresistance is vital for developing effective cancer treatments.
Purpose of the Study:
- To investigate the relationship between miR-206 expression and chemoresistance in papillary thyroid carcinoma (PTC).
- To explore the potential of miR-206 as a regulator of euthyrox resistance in PTC cells.
Main Methods:
- Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) to assess miR-206 expression.
- Cell viability, proliferation, and apoptosis assays (CCK-8, EdU, flow cytometry) were performed.
- Luciferase reporter assays and Western blotting were used to identify targets and protein expression.
Main Results:
- miR-206 was significantly downregulated in PTC tissues and euthyrox-resistant cell lines.
- Overexpression of miR-206 decreased IC50 values, inhibited proliferation, induced apoptosis, and suppressed multidrug resistance proteins.
- miR-206 targets MAP4K3, negatively regulating its expression and subsequently inhibiting p38 and JNK signaling pathways.
Conclusions:
- miR-206 plays a key role in euthyrox resistance in PTC by targeting MAP4K3 and inhibiting p38 and JNK signaling.
- Restoring miR-206 levels presents a potential therapeutic strategy for euthyrox-resistant PTC.
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