DCAF1 interacts with PARD3 to promote hepatocellular carcinoma progression and metastasis by activating the Akt signaling pathway
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Le résumé fourni par la source
BACKGROUND: Hepatocellular carcinoma (HCC) is a fatal malignancy with poor prognosis due to lack of effective clinical interference. DCAF1 plays a vital role in regulating cell growth and proliferation, and is involved in the progression of various malignancies. However, the function of DCAF1 in HCC development and the underlying mechanism are still unknown. This study aimed to explore the effect of DCAF1 in HCC and the corresponding molecular mechanism. METHODS: Quantitative real-time PCR, Western blot and immunostaining were used to determine DCAF1 expression in tumor tissues and cell lines. Subsequently, in vitro and in vivo experiments were conducted to explore the function of DCAF1 in tumor growth and metastasis in HCC. Coimmunoprecipitation, mass spectrometry and RNA sequencing were performed to identify the underlying molecular mechanisms. RESULTS: In this study, we found that DCAF1 was observably upregulated and associated with poor prognosis in HCC. Knockdown of DCAF1 inhibited tumor proliferation and metastasis and promoted tumor apoptosis, whereas overexpressing DCAF1 yielded opposite effects. Mechanistically, DCAF1 could activate the Akt signaling pathway by binding to PARD3 and enhancing its expression. We also found that the combined application of DCAF1 knockdown and Akt inhibitor could significantly suppress subcutaneous xenograft tumor growth. CONCLUSIONS: Our study illustrates that DCAF1 plays a crucial role in HCC development and the DCAF1/PARD3/Akt axis presents a potentially effective therapeutic strategy for HCC.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- DCAF1 interacts with PARD3 to promote hepatocellular carcinoma progression and metastasis by activating the Akt signaling pathway
- Date Crossref
- 06/05/2024
- Éditeur
- Springer Science and Business Media LLC
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Chinese Academy of Medical Sciences & Peking Union Medical College Department of Hepatobiliary Surgery pays non établi dans la noticeUniversité ou école supérieure
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Peking Union Medical College Hospital pays non établi dans la noticeÉtablissement de santé
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Nanjing Drum Tower Hospital Department of Hepatobiliary Surgery pays non établi dans la noticeÉtablissement de santé
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Anhui Medical University Department of Hepatobiliary Surgery pays non établi dans la noticeUniversité ou école supérieure
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First Affiliated Hospital of Anhui Medical University pays non établi dans la noticeÉtablissement de santé
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The Affiliated Drum Tower Hospital of Nanjing University Medical School Department of Hepatobiliary Surgery pays non établi dans la noticeUniversité ou école supérieure
Department of Hepatobiliary Surgery — Chinese Academy of Medical Sciences & Peking Union Medical College, Peking Union Medical College Hospital et Department of Hepatobiliary Surgery — Nanjing Drum Tower Hospital, avec 3 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.