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Background <p>SUGT1 (Suppressor of the G2 allele of SKP1) and FH (fumarate hydratase) have recently garnered significant attention from the research community. SUGT1 functions as a molecular chaperone, regulating the stability and activity of various proteins, while FH is a key enzyme in the tricarboxylic acid cycle, catalyzing the reversible conversion of fumarate to malate. Existing literature has established their essential roles in signaling, tumorigenesis, and cancer progression. However, their functions and mechanisms in ovarian cancer (OC) remain poorly understood.</p> Results <p>We found that high SUGT1 expression is associated with a more advanced FIGO stage in OC. SUGT1 knockdown significantly inhibits OC cell proliferation and metastasis, while its overexpression has the opposite oncogenic effect. Mechanistically, we revealed that SUGT1 promotes FH protein degradation via the ubiquitin-proteasome pathway. Moreover, FH knockdown partly reversed the inhibitory effects of SUGT1 knockdown on tumor cell proliferation, migration, and proteins of phosphorylated PI3K/AKT and Vimentin. In summary, We demonstrated that SUGT1 exerts oncogenic functions in OC by regulating FH stability.</p> Conclusions <p>Our study is the first to provide experimental evidence elucidating the SUGT1-FH relation and its role in OC progression, offering potential significance for clinical diagnosis and therapy.</p>

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Mechanism by which SUGT1 downregulates FH to promote proliferation and migration in serous ovarian cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月29日

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  • Tianli Mu,
  • Bo Ren,
  • Ziteng Kuang,
  • Runze He,
  • Bingjie Rui,
  • Ye Yang,
  • Yuxi Liu,
  • Danbo Geng,
  • Yuci Zhang,
  • Min Wang

摘要

Background

SUGT1 (Suppressor of the G2 allele of SKP1) and FH (fumarate hydratase) have recently garnered significant attention from the research community. SUGT1 functions as a molecular chaperone, regulating the stability and activity of various proteins, while FH is a key enzyme in the tricarboxylic acid cycle, catalyzing the reversible conversion of fumarate to malate. Existing literature has established their essential roles in signaling, tumorigenesis, and cancer progression. However, their functions and mechanisms in ovarian cancer (OC) remain poorly understood.

Results

We found that high SUGT1 expression is associated with a more advanced FIGO stage in OC. SUGT1 knockdown significantly inhibits OC cell proliferation and metastasis, while its overexpression has the opposite oncogenic effect. Mechanistically, we revealed that SUGT1 promotes FH protein degradation via the ubiquitin-proteasome pathway. Moreover, FH knockdown partly reversed the inhibitory effects of SUGT1 knockdown on tumor cell proliferation, migration, and proteins of phosphorylated PI3K/AKT and Vimentin. In summary, We demonstrated that SUGT1 exerts oncogenic functions in OC by regulating FH stability.

Conclusions

Our study is the first to provide experimental evidence elucidating the SUGT1-FH relation and its role in OC progression, offering potential significance for clinical diagnosis and therapy.