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Increased KCNQ3 expression in papillary thyroid cancer promotes proliferation and migration
Qiuli Li1,2, Muyuan Liu3, Xuhong Song2
1Department of Central Laboratory, Cancer Hospital of Shantou University Medical College, Shantou, China.
Cancer Cell International
|November 18, 2025
Summary
Papillary thyroid cancer (PTC) involves overexpressed KCNQ3, driving proliferation and migration. Estradiol regulates KCNQ3, explaining gender bias, and the inhibitor XE991 shows therapeutic potential for PTC.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Papillary thyroid cancer (PTC) incidence is rising globally.
- KCNQ3 is overexpressed in PTC, but its oncogenic role is unclear.
Purpose of the Study:
- Elucidate the oncogenic mechanism of KCNQ3 in PTC.
- Investigate KCNQ3's role in tumor progression and potential therapeutic targets.
Main Methods:
- Assessed KCNQ3 expression using GEPIA, IHC, and Western blotting.
- Evaluated KCNQ3 function via in vitro/in vivo assays and protein interaction studies (co-IP, MS).
- Examined estradiol (E2)-mediated regulation via ChIP-qPCR and tested KCNQ3 inhibitor XE991.
Main Results:
- KCNQ3 upregulation in PTC promotes tumor cell proliferation and migration.
- KCNQ3 activates the RAS/RAF/MAPK pathway by interacting with GAREM1, GRB2, and SOS1.
- Estradiol enhances KCNQ3 transcription via ESR1 binding, and XE991 inhibits PTC cell growth.
Conclusions:
- Identified a novel KCNQ3-driven oncogenic axis in PTC, highlighting KCNQ3 as a therapeutic target.
- Established E2 as a KCNQ3 regulator, explaining PTC's female gender bias.
- Demonstrated XE991's potential for PTC treatment.
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