ArticleDiscover oncology2026
Pan-cancer investigation identifies ARL4A as a prospective therapeutic indicator for thyroid cancer.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
backgroundADP-ribosylation factor-like 4 A (ARL4A), a small GTPase involved in cytoskeletal dynamics and signal transduction, exhibits dysregulated expression in various cancers, yet its comprehensive role across tumor types, particularly in thyroid carcinoma (THCA), remains underexplored. This study aimed to perform a systematic pan-cancer analysis of ARL4A to elucidate its expression patterns, prognostic implications, genetic and epigenetic alterations, immune correlations, drug sensitivity, and functional contributions to THCA progression.
methodsLeveraging multi-omics data from TCGA and tools including TIMER2.0, GEPIA2, UALCAN, cBioPortal, and LinkedOmics, we evaluated ARL4A across 33 cancer types. Functional validation was conducted by overexpressing ARL4A in THCA cell lines (BCPAP and KTC-1), with assessments via Western blotting, CCK-8 proliferation assays, wound healing, and Transwell migration assays.
resultsARL4A mRNA levels were significantly reduced in tumors such as THCA, correlating with early stages in some cancers but poor overall survival in THCA, adrenocortical carcinoma, and bladder cancer. Genetic amplifications predominated, alongside promoter hypomethylation in multiple malignancies. ARL4A expression inversely correlated with CD8 + T cells and other antitumor infiltrates while positively associating with myeloid-derived suppressor cells and immunosuppressive chemokines. Drug sensitivity analysis revealed negative correlations with HSP90 inhibitors. In THCA cells, ARL4A overexpression enhanced proliferation, migration, and epithelial-mesenchymal transition markers (N-cadherin and Vimentin).
conclusionsThese results establish ARL4A as an oncogenic promoter in THCA through modulation of proliferation, migration, and immunosuppressive microenvironments, positioning it as a promising prognostic biomarker and therapeutic target for precision oncology.
Indexed as
Identifiers
What OpenQuestion holds
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.