Evidence map›Paper›PMID 40155591›Full record

ArticleCell death & disease2025

CSF3R-AS promotes hepatocellular carcinoma progression and sorafenib resistance through the CSF3R/JAK2/STAT3 positive feedback loop.

Ziyang Feng, Yan Gao, Changjing Cai, Jun Tan, Ping Liu, Yihong Chen, Gongping Deng, Yanhong Ouyang, Xuewen Liu, Ke Cao and 4 more

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

14 authors.

Ziyang FengDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Yan GaoDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Changjing CaiDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Jun TanDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Ping LiuDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Yihong ChenDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Gongping DengDepartment of Emergency, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan, 570311, China.
Yanhong OuyangDepartment of Emergency, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan, 570311, China.
Xuewen LiuDepartment of Oncology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Ke CaoDepartment of Oncology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Shan ZengDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.ORCID http://orcid.org/0000-0002-0988-723X
Ying HanDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Xiangying DengDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Hong ShenDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China. hongshen2000@csu.edu.cn.ORCID http://orcid.org/0000-0002-6456-8231

Funding

China Postdoctoral Science Foundation 2023JJ40942China Postdoctoral Science Foundation 2024M753681National Natural Science Foundation of China (National Science Foundation of China) 82373275, 81974384, 82173342 & 82203015National Natural Science Foundation of China (National Science Foundation of China) 82403854
6 · The paper itself

Abstract

Antisense circular RNA is a special type of circular RNA that is derived from the antisense complementary strand of parental mRNA. However, the function of antisense circRNA in hepatocellular carcinoma (HCC) is still unclear. Here, we reported that CSF3R-AS was upregulated in HCC and correlated with a poor prognosis. CSF3R-AS promoted the proliferation, angiogenesis, and metastasis of HCC, and inhibited apoptosis. Mechanistically, CSF3R-AS has a 180-base complementary pairing sequence with its parental mRNA CSF3R, which can directly bind to CSF3R and recruit RBMS3 to stabilize its parental mRNA, and finally activate JAK2/STAT3 signaling pathway. Interestingly, STAT3 can act as a transcription factor of CSF3R-AS, which means that there is a CSF3R-AS/CSF3R/JAK2/STAT3 positive feedback loop in HCC. Finally, the CSF3R-AS/CSF3R/JAK2/STAT3 positive feedback loop was also activated in HCC sorafenib-resistant cells, and blocking this loop was expected to improve the sensitivity of HCC to sorafenib. These findings suggested that the CSF3R-AS/CSF3R/JAK2/STAT3 positive feedback loop could promote HCC progression and sorafenib resistance. Blocking this loop is expected to provide new research directions and therapy targets for HCC.

Indexed as

Carcinoma, HepatocellularDrug Resistance, NeoplasmJanus Kinase 2Liver NeoplasmsReceptors, Colony-Stimulating FactorSorafenibSTAT3 Transcription FactorAnimalsApoptosisCell Line, TumorCell ProliferationDisease ProgressionFeedback, PhysiologicalFemaleGene Expression Regulation, NeoplasticHumansJAK2 protein, humanJanus Kinase 2Receptors, Colony-Stimulating FactorRNA, CircularSorafenibSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID40155591
PMCPMC11953311

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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.