Evidence map›Paper›PMID 39849382›Full record

ArticleMolecular medicine (Cambridge, Mass.)2025

AdipoR1 enhances the radiation resistance via ESR1/CCNB1IP1/cyclin B1 pathway in hepatocellular carcinoma cells.

Yuhan Gan, Linhui Zhu, Yimo Li, Ruoting Ge, Jiahe Tian, Yuxin Chen, Xiang He, Shumei Ma, Xiaodong Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Yuhan Gan *School of Public Health, Wenzhou Medical University, Wenzhou, 325035, China.
Linhui Zhu *School of Public Health, Wenzhou Medical University, Wenzhou, 325035, China.
Yimo Li *School of Public Health, Wenzhou Medical University, Wenzhou, 325035, China.
Ruoting GeSchool of Public Health, Wenzhou Medical University, Wenzhou, 325035, China.
Jiahe TianSchool of Public Health, Wenzhou Medical University, Wenzhou, 325035, China.
Yuxin ChenSchool of Public Health, Wenzhou Medical University, Wenzhou, 325035, China.
Xiang HeSchool of Public Health, Wenzhou Medical University, Wenzhou, 325035, China.
Shumei MaSchool of Public Health, Wenzhou Medical University, Wenzhou, 325035, China. Shmm2001@126.com.
Xiaodong LiuSchool of Public Health, Wenzhou Medical University, Wenzhou, 325035, China. liuxd2014@126.com.

Funding

National Innovation and Entrepreneurship Training Program for College Students No. 202210343013National Natural Science Foundation of China Nos. 81972969Zhejiang Provincial Basic Public Welfare Research Program LY23H220001
6 · The paper itself

Abstract

Hepatocellular carcinoma is one of the most common malignant tumors, and radiotherapy plays a pivotal role in its therapeutic regimen. However, radiotherapy resistance is the main cause of therapeutic failure in patients. Our previous study revealed that Adiponectin Receptor 1 (AdipoR1) is involved in regulating radiation resistance in liver cancer patients treated with stereotactic body radiotherapy. To explore the mechanism, we performed high-throughput transcriptome sequencing of hepatocellular carcinoma cells with stable knockdown of AdipoR1. KEGG enrichment analysis indicated that the cell cycle and ubiquitination degradation pathways may be involved in the regulation of radiation resistance by AdipoR1.The knockdown of AdipoR1 can attenuate the radiation-induced G2/M phase arrest through cyclin B1.By the ubiquitination IP assay and a rescue experiment, we confirmed that CCNB1IP1 regulated the ubiquitination and degradation of cyclin B1. Combined with information from transcription factor database and AdipoR1 transcriptome sequencing, these results showed that estrogen receptor 1 (ESR1) may be a transcription factor of CCNB1IP1. We found that AdipoR1 promoted the translocation of ESR1 from the cytoplasm to the nucleus, and ESR1 inhibited the transcription of CCNB1IP1.Therefore, we propose that AdipoR1 regulates the ubiquitination level, cell cycle progression, and radiation resistance of HCC cells through the "AdipoR1 /ESR1/CCNB1IP1/cyclin B1" axis. This study will promote the development of novel targeted radiosensitizing drugs.

Indexed as

Carcinoma, HepatocellularCyclin B1Liver NeoplasmsRadiation ToleranceReceptors, AdiponectinCell Line, TumorEstrogen Receptor alphaGene Expression Regulation, NeoplasticHep G2 CellsHumansSignal TransductionUbiquitinationADIPOR1 protein, humanCCNB1 protein, humanCyclin B1ESR1 protein, humanEstrogen Receptor alphaReceptors, AdiponectinAdipoR1CCNB1IP1Cell cycleCyclin B1HCCRadiation resistance

Identifiers

PMID39849382
PMCPMC11755959

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.