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Potential Anti-Cancer Drug 6RK73 Suppresses Ovarian Cancer Growth by Inactivating the AKT1/Sp1 Induced c-Myc
Sisi Kuang1,2, Weifeng Feng3, Siqi He4
1Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
Journal of Cancer
|January 26, 2026
Summary
The novel drug 6RK73 shows anti-cancer effects in ovarian cancer by inhibiting the AKT1/Sp1/c-Myc pathway. This promising agent suppresses tumor growth and proliferation, offering potential for new ovarian cancer treatments.
Area of Science:
- Oncology
- Pharmacology
Background:
- 6RK73 is a novel drug targeting UCHL1 deubiquitinase with preliminary anti-cancer activity.
- Its efficacy in ovarian cancer is not yet established.
Purpose of the Study:
- To investigate the anti-cancer effects and mechanism of 6RK73 in ovarian cancer.
- To determine the drug's IC50 values in ovarian cancer cell lines.
Main Methods:
- Determined IC50 values in OVCAR3 and SKOV3 ovarian cancer cell lines.
- Assessed 6RK73's effects on cell proliferation, cell cycle, and tumor formation in vivo.
- Investigated the impact on the AKT1/Sp1/c-Myc signaling pathway.
Main Results:
- 6RK73 demonstrated significant inhibition of ovarian cancer cell proliferation and tumor growth.
- The drug effectively arrested cell cycle progression in vitro.
- Mechanistically, 6RK73 inhibited the AKT1/Sp1/c-Myc pathway, reducing c-Myc expression independently of UCHL1.
- AKT1 overexpression counteracted 6RK73's effects.
Conclusions:
- 6RK73 is a potential anti-cancer agent for ovarian cancer.
- Its mechanism involves inactivation of the AKT1/Sp1/c-Myc signaling pathway.
- The anti-tumor effects are independent of UCHL1 inhibition.
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