ArticleThe Journal of clinical investigation2022
BCL6 is regulated by the MAPK/ELK1 axis and promotes KRAS-driven lung cancer.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- FTO-mediated mRNA biology · 2026Article
- DUSP5 suppresses esophageal squamous cell carcinoma by counteracting macrophage-derived AREG-ERK1/2 signaling and disrupting an oncogenic ERK1/2-ELK1-DUSP5 feedback circuitry.Cell death & disease · 2026Article
- ELK1 promotes the progress of myeloid leukemia by hindering the differentiation of neutrophils.Experimental hematology & oncology · 2026Article
- miR-2110 orchestrates ERK-ELK1 transcriptional repression to induce cell-cycle arrest and enhance cytarabine sensitivity in acute myeloid leukemia.Frontiers in oncology · 2026Article
- Novel Small Molecule DZ-865B Effectively Degrades BCL6, Promotes Apoptosis and Reduces Proliferation of Diffuse Large B-Cell Lymphoma Cells.Oncology research · 2026Article
- Role of signaling pathways in lung cancer development and advances in targeted therapies (Review).Oncology letters · 2025Review
- Molecular signatures under hexavalent chromium, particulate matter 2.5, and cigarette smoking exposures.Discover oncology · 2025Article
- Mechanistic Insights and Clinical Implications of ELK1 in Solid Tumors: A Narrative Review.Cells · 2025Review
- Shared blood gene signature in lung adenocarcinoma and microbial lung infections: a bioinformatic analysis and in silico validation.Discover oncology · 2025Article
- KRAS/PI3K axis driven GTF3C6 expression and promotes LUAD via FAK pathway.Journal of advanced research · 2025Article
- FLLL31 Induces Apoptosis via the FOXO4/BCL6 Axis to Inhibit Bladder Cancer Progression.Human mutation · 2025Article
- BCL6 promotes the progression of high-grade serous ovarian cancer cells by inhibiting PLAAT4.Frontiers in pharmacology · 2025Article
- B Cell Lymphoma 6 (BCL6): A Conserved Regulator of Immunity and Beyond.International journal of molecular sciences · 2024Review
- Transcriptomic analysis reveals transcription factors implicated in radon-induced lung carcinogenesis.Toxicology research · 2024Article
- Application and research progress of cordycepin in the treatment of tumours (Review).Molecular medicine reports · 2024Review
- Circular RNAs in human diseases.MedComm · 2024Review
- The HOXC10/NOD1/ERK axis drives osteolytic bone metastasis of pan-KRAS-mutant lung cancer.Bone research · 2024Article
- Highly expressed of BID indicates poor prognosis and mediates different tumor microenvironment characteristics in clear cell renal cell carcinoma.Discover oncology · 2024Article
- Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis.Nature communications · 2024Article
- Elk1 enhances inflammatory cell infiltration and exacerbates acute lung injury/acute respiratory distress syndrome by suppressing Fcgr2b transcription.Molecular medicine (Cambridge, Mass.) · 2024Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutational activation of KRAS is a common oncogenic event in lung cancer, yet effective therapies are still lacking. Here, we identify B cell lymphoma 6 (BCL6) as a lynchpin in KRAS-driven lung cancer. BCL6 expression was increased upon KRAS activation in lung tumor tissue in mice and was positively correlated with the expression of KRAS-GTP, the active form of KRAS, in various human cancer cell lines. Moreover, BCL6 was highly expressed in human KRAS-mutant lung adenocarcinomas and was associated with poor patient survival. Mechanistically, the MAPK/ERK/ELK1 signaling axis downstream of mutant KRAS directly regulated BCL6 expression. BCL6 maintained the global expression of prereplication complex components; therefore, BCL6 inhibition induced stalling of the replication fork, leading to DNA damage and growth arrest in KRAS-mutant lung cancer cells. Importantly, BCL6-specific knockout in lungs significantly reduced the tumor burden and mortality in the LSL-KrasG12D/+ lung cancer mouse model. Likewise, pharmacological inhibition of BCL6 significantly impeded the growth of KRAS-mutant lung cancer cells both in vitro and in vivo. In summary, our findings reveal a crucial role of BCL6 in promoting KRAS-addicted lung cancer and suggest BCL6 as a therapeutic target for the treatment of this intractable disease.
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