ArticleJournal of molecular histology2025
FAM64A regulates the malignant phenotype and tumor microenvironment of non-small cell lung cancer by activating the JAK/STAT3/PDL1 axis.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Solasonine suppresses non-small cell lung cancer progression by inhibiting the STAT3/PD-L1 axis.Scientific reports · 2026Article
- Fortunellin's dual role in mitigating ferroptosis and neuroinflammation in cerebral ischemia/reperfusion injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) is a life-threatening disease that still lacks effective targeted treatment. Family with sequence similarity 64, member A (FAM64A) is dysregulated in different malignancies and participates in the cancer progression. To address the role of FAM64A in NSCLC. The FAM64A expression was detected by reverse transcription quantitative polymerase chain reaction and western blotting. Short-hairpin RNAs (shRNAs) against FAM64A were transfected into A549 and H460 cells. The role of FAM64A in vitro was evaluated by cell counting kit-8, transwell, enzyme-linked immunosorbent assay, immunofluorescence and western blotting. In vivo role of FAM64A was addressed in xenografted mice using immunohistochemistry and western blotting. FAM64A was upregulated in NSCLC that predicted a dismal prognosis for NSCLC patients. Knockdown of FAM64A diminished cell viability, invaded cell numbers, the Vimentin expression and the concentrations of TGF-β and IL-10, but fostered the E-cadherin expression and the concentrations of IL-2 and IFN-γ in NSCLC cells. Mechanistically, silencing of FAM64A declined the expression of JAK/STAT3/PD-L1 pathway, which was restored with the application of RO8191, an activator of JAK/STAT3 pathway. The inhibitory role of FAM64A knockdown in NSCLC cell proliferation, invasion, EMT and immune escape was inverted by the management of RO8191. In vivo, knockdown of FAM64A reduced tumor size and weight, the level of Vimentin and PD-L1, and the expression of JAK/STAT3/PD-L1 pathway, but enhanced the IFN-γ level. Upregulation of FAM64A promoted proliferation, invasion, EMT and immune escape through activating JAK/STAT3/PD-L1 axis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.