Evidence map›Paper›PMID 41312719›Full record

ArticleInternational journal of oncology2026

c‑Myc‑regulated RPLP0 via the ROS‑mediated JAK2/STAT3 positive feedback loop facilitates hepatocellular carcinoma malignancy progression.

Yanqiu Meng, Lebin Yuan, Gangrui Meng, Hongxiang Huang, Xianbin Huang, Xinping Xu, Xiaodong Peng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Experimental and therapeutic medicine · 2026
    Article
  2. Article
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

7 authors.

Yanqiu Meng *Department of Oncology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Lebin Yuan *Department of Thyroid and Breast Surgery, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang Central Hospital, Xiangyang, Hubei 441000, P.R. China.
Gangrui Meng *Department of General Surgery, First Clinical College, Hubei University of Medicine, Shiyan, Hubei 442000, P.R. China.
Hongxiang HuangDepartment of Oncology, Ganzhou Hospital‑Nanfang Hospital, Southern Medical University, Ganzhou, Jiangxi 341000, P.R. China.
Xianbin HuangDepartment of Oncology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Xinping XuJiangxi Provincial Key Laboratory of Respiratory Diseases, Jiangxi Institute of Respiratory Diseases, The Department of Respiratory and Critical Care Medicine, Jiangxi Clinical Research Center for Respiratory Diseases, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Xiaodong PengDepartment of Oncology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) continues to rank as a predominant contributor to cancer‑related mortality on a global scale, attributed to its insidious onset and unfavorable prognosis. The ribosomal protein lateral stalk subunit P0 (RPLP0) has recently gathered widespread attention as a crucial factor in the pathological progression of various neoplasms; however, its exact role in HCC remains inadequately defined. Consequently, the present study endeavored to shed light on the function and mechanistic underpinnings of RPLP0 in HCC and assess its clinical significance and potential as a therapeutic target. qPCR and western blot analyses indicated that RPLP0 was markedly upregulated in HCC, with its elevated levels correlating with poorer survival outcomes. Silencing RPLP0 expression suppressed the proliferative, invasive, migratory, and epithelial‑mesenchymal transition (EMT) abilities of HCC cells, while concurrently promoting apoptosis, autophagy, and G

Indexed as

Carcinoma, HepatocellularJanus Kinase 2Liver NeoplasmsProto-Oncogene Proteins c-mycRibosomal ProteinsSTAT3 Transcription FactorApoptosisCell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFeedback, PhysiologicalFemaleGene Expression Regulation, NeoplasticHumansJAK2 protein, humanJanus Kinase 2MYC protein, humanProto-Oncogene Proteins c-mycReactive Oxygen SpeciesRibosomal ProteinsSTAT3 protein, humanSTAT3 Transcription Factorc‑Mychepatocellular carcinomaJAK2/STAT3reactive oxygen speciesribosomal protein lateral stalk subunit P0

Identifiers

PMID41312719
PMCPMC12674198

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.