ArticleCancer letters2022
BAP1 maintains HIF-dependent interferon beta induction to suppress tumor growth in clear cell renal cell carcinoma.
Article in Cancer letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Deubiquitinating enzymes in kidney diseases: Molecular mechanisms, pathological roles and therapeutic opportunities (Review).Molecular medicine reports · 2026Review
- Deep visual multi-omics profiling links morphology and molecular programs in clear cell renal cell carcinoma.EMBO molecular medicine · 2026Article
- BAP1 deficiency-induced SKA3 promotes clear cell renal cell carcinoma malignant progression by regulating chromosomal instability.Cell death & disease · 2026Article
- From energy metabolic homeostasis to immune remodeling: the role and therapeutic potential of STING signaling in the tumor microenvironment.Cell communication and signaling : CCS · 2026Review
- BAP1 dysregulation impairs trophoblast differentiation and contributes to placental dysfunction in preeclampsia.Cell death & disease · 2026Article
- Functional characterization of BAP1 mutations in genome edited cholangiocarcinoma organoids: Role in cell death and drug responses.iScience · 2026Article
- VHL synthetic lethality screens uncover CBF-β as a negative regulator of STING.Nature communications · 2026Article
- LDRT combined with anti-PD-1 promotes tumor regression in head and neck squamous cell carcinoma through tumor metaprogram evolution and immune cell reprogramming.Journal of experimental & clinical cancer research : CR · 2026Article
- LAC-TME classifier: machine learning-driven model predicts survival and prioritizes targeted therapy in clear cell renal cell carcinoma.Journal of cancer research and clinical oncology · 2025Article
- BAP1 as a predictive biomarker of therapeutic response to oncolytic vaccinia virus for metastatic renal cell carcinoma therapy.Cancer immunology, immunotherapy : CII · 2025Article
- Gene profiling and clinicopathological features for prognostic modeling of recurrence in non-metastatic clear-cell renal cell carcinoma.Translational andrology and urology · 2025Article
- The fall of the genome protectors triad: PBRM1, SETD2, and BAP1's impact on metabolism and immunity in clear cell renal cell carcinoma.Frontiers in cell and developmental biology · 2025Review
- Understanding the intersection between placental development and cancer: Lessons from the tumor suppressor BAP1.Communications biology · 2024Review
- Article
- The 5th Kidney Cancer Research Summit: Research Accelerating Cures for Renal Cell Carcinoma in 2023.The oncologist · 2024Article
- PD-1 inhibitor plus oncolytic vaccinia virus is a safe and effective treatment option for metastatic renal cell carcinoma.Cancer cell international · 2024Article
- Dysregulation of ubiquitination modification in renal cell carcinoma.Frontiers in genetics · 2024Review
- The SIRT7-mediated deacetylation of CHD1L amplifies HIF-2α-dependent signal that drives renal cell carcinoma progression and sunitinib resistance.Cell & bioscience · 2023Article
- Data supporting the roles of BAP1, STING, and IFN-β in ISGF3 activation in ccRCC.Data in brief · 2022Article
- The convergence of tumor suppressors on the type I interferon pathway in clear cell renal cell carcinoma and its therapeutic implications.American journal of physiology. Cell physiology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
BRCA1-associated protein 1 (BAP1) is a deubiquitinase that is mutated in 10-15% of clear cell renal cell carcinomas (ccRCC). Despite the association between BAP1 loss and poor clinical outcome, the critical tumor suppressor function(s) of BAP1 in ccRCC remains unclear. Previously, we found that hypoxia-inducible factor 2α (HIF2α) and BAP1 activate interferon-stimulated gene factor 3 (ISGF3), a transcription factor activated by type I interferons and a tumor suppressor in ccRCC xenograft models. Here, we aimed to determine the mechanism(s) through which HIF and BAP1 regulate ISGF3. We found that in ccRCC cells, loss of the von Hippel-Lindau tumor suppressor (VHL) activated interferon beta (IFN-β) expression in a HIF2α-dependent manner. IFN-β was required for ISGF3 activation and suppressed the growth of Ren-02 tumors in xenografts. BAP1 enhanced the expression of IFN-β and stimulator of interferon genes (STING), both of which activate ISGF3. Both ISGF3 overexpression and STING agonist treatment increased ISGF3 activity and suppressed BAP1-deficient tumor growth in Ren-02 xenografts. Our results indicate that BAP1 loss reduces type I interferon signaling, and reactivating this pathway may be a novel therapeutic strategy for treating ccRCC.
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