Transcription factor ZNF266 suppresses cancer progression by modulating CA9-mediated intracellular pH alteration in lung adenocarcinoma
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View abstract on PubMed
Summary
This summary is machine-generated.ZNF266, a transcription factor, inhibits lung adenocarcinoma (LUAD) progression by suppressing CA9 expression, impacting pH and mTOR signaling. Overexpressing ZNF266 shows therapeutic potential for LUAD treatment.
Area Of Science
- Oncology
- Molecular Biology
- Cancer Genetics
Background
- Lung adenocarcinoma (LUAD) is a leading cause of cancer mortality.
- The role of transcription factors in LUAD progression is not well understood.
- ZNF266's function in LUAD has not been previously investigated.
Purpose Of The Study
- To investigate the role of ZNF266 in LUAD progression.
- To elucidate the molecular mechanisms underlying ZNF266's function in LUAD.
- To evaluate the therapeutic potential of ZNF266 in LUAD.
Main Methods
- Analysis of high-throughput sequencing data and retrospective patient data.
- Functional studies in cell lines, organoids, and xenograft models.
- RNA sequencing, ChIP, DNA pull-down, dual-luciferase assays, and AAV-mediated gene delivery.
Main Results
- ZNF266 is downregulated in LUAD and associated with poor prognosis.
- ZNF266 inhibits LUAD cell proliferation, migration, and invasion.
- ZNF266 suppresses CA9 transcription, reducing intracellular pH and inhibiting mTOR signaling.
Conclusions
- ZNF266 inhibits LUAD progression in a pH-dependent manner by modulating CA9.
- ZNF266 demonstrates therapeutic potential for LUAD treatment.
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