Evidence map›Paper›PMID 42010436›Full record

ArticleBiology direct2026

Inhibition of circZFX suppresses malignant phenotypes in cholangiocarcinoma via the miR-654-3p/HDGF and YAP1 signaling activation.

Tingming Liang, Chengxuan Gong, Xinbing Yang, Jie Shen, Guijie Jiang, Jiarui Liu, Guang Yang, Li Guo

Abstract read
In one paragraph

Article in Biology direct, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Tingming LiangSchool of Life Science, Nanjing Normal University, Nanjing, 210023, China.ORCID http://orcid.org/0000-0002-6421-0010
Chengxuan GongSchool of Life Science, Nanjing Normal University, Nanjing, 210023, China.
Xinbing YangSchool of Life Science, Nanjing Normal University, Nanjing, 210023, China.
Jie ShenSchool of Life Science, Nanjing Normal University, Nanjing, 210023, China.
Guijie JiangSchool of Life Science, Nanjing Normal University, Nanjing, 210023, China.
Jiarui LiuState Key Laboratory of Flexible Electronics (LoFE), School of Chemistry and Life Sciences, Nanjing University of Posts and Telecommunications, Nanjing, 210023, China.
Guang YangSchool of Life Science, Nanjing Normal University, Nanjing, 210023, China.
Li GuoState Key Laboratory of Flexible Electronics (LoFE), School of Chemistry and Life Sciences, Nanjing University of Posts and Telecommunications, Nanjing, 210023, China. lguo@njupt.edu.cn.

Funding

National Natural Science Foundation of China 62571264 and 62171236the key project of social development in Jiangsu Province BE2022799the key projects of Natural Science Research in Universities of Jiangsu Province 22KJA180006
6 · The paper itself

Abstract

Cholangiocarcinoma (CCA) is a highly aggressive hepatobiliary malignancy by a poor prognosis. circular RNAs (circRNAs) have poorly characterized roles in CCA. This study identified that circZFX was significantly upregulated in 4 CCA cell lines and 20 paired CCA/normal tissues. circZFX knockdown suppressed CCA proliferation, migration, and invasion in vitro and reduced xenograft tumor volume by 57% in vivo. Mechanistically, circZFX functions as a competing endogenous RNA for miR-654-3p, thus derepressing HDGF. miR-654-3p inhibitor could reverse the inhibitory effects on the proliferation activity, migration, and invasion capabilities of HuCCT1 and QBC939 cells caused by circZFX silencing. Importantly, co-immunoprecipitation revealed HDGF interaction with YAP1, and circZFX knockdown downregulated YAP1 expression. These findings indicate that inhibition of circZFX suppresses malignant phenotypes in cholangiocarcinoma via the miR-654-3p/HDGF and YAP1 signaling activation, highlighting this axis as a novel therapeutic target and providing mechanistic insights for molecular subtyping and the development of circRNA-based precision therapeutics.

Indexed as

Adaptor Proteins, Signal TransducingBile Duct NeoplasmsCholangiocarcinomaIntercellular Signaling Peptides and ProteinsMicroRNAsRNA, CircularTranscription FactorsAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMiceSignal TransductionYAP-Signaling ProteinsAdaptor Proteins, Signal Transducinghepatoma-derived growth factorIntercellular Signaling Peptides and ProteinsMicroRNAsRNA, CircularTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsCholangiocarcinoma (CCA)CircZFXHDGFmiR-654-3pYAP1

Identifiers

PMID42010436
PMCPMC13227891

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Registered trials

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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.