ArticleCell death & disease2026
VIRMA/IGF2BP3-mediated ANLN upregulation promotes intrahepatic cholangiocarcinoma growth by forming a positive feedback loop with RhoA/YAP1/TEAD1 signaling pathway.
Article in Cell death & disease, 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
7 authors.
Funding
Abstract
The prognosis of patients with intrahepatic cholangiocarcinoma (ICC) remains poor owing to the lack of effective targeted therapeutic strategies. Thus, the exploration of the molecular pathogenesis of ICC is urgently required. The cytoskeleton protein, anillin (ANLN), has been reported to contribute to various tumor growth by participating in cytokinesis via RhoA signaling. However, the exact physiological role and potential regulatory mechanism of ANLN in ICC are still not well understood. Based on spindle-related genes, integrated bioinformatic analyses identified ANLN as a potential candidate target for ICC. ANLN was elevated in ICC and predicted worse survival. Mechanistically, VIRMA-mediated m6A modification and IGF2BP3-dependent interaction collectively accounted for the upregulation of ANLN by maintaining its mRNA stability. Furthermore, the combination of ANLN and VIRMA or IGF2BP3 offered a greater predictive value than each marker alone in a large ICC cohort. Functional studies indicated that ANLN was involved in cancer cell proliferation and cell cycle. ANLN knockdown induced cytokinesis failure, DNA damage, and apoptosis in ICC cells. In addition to discovering the crucial role of ANLN in cytokinesis via RhoA activation, we also illustrated that ANLN restrained the Hippo pathway by enhancing the activity of RhoA signaling, which together contributed to ANLN-mediated tumor-promoting effects on ICC. Furthermore, YAP1-TEAD1 transcriptionally activated ANLN, subsequently establishing a self-reinforcing loop between ANLN and Hippo pathway, which was mediated by RhoA signaling as an intermediate regulatory node. Importantly, two clinical drugs, the RhoA inhibitor simvastatin and the YAP1/TEAD inhibitor verteporfin were determined to be the disruptors of this feed-forward signaling axis, inhibiting ICC tumor growth. These findings reveal the vital function of ANLN in ICC growth and provide promising treatment strategies for ICC.
Indexed as
Identifiers
What Socratic 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 Socratic graph.