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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
PubMed

Insights

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.
Keywords:
6RK73AKT1Sp1UCHL1c-Mycovarian cancer

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