Evidence map›Paper›PMID 34526098›Full record

ArticleJournal of experimental & clinical cancer research : CR2021

circHMGCS1-016 reshapes immune environment by sponging miR-1236-3p to regulate CD73 and GAL-8 expression in intrahepatic cholangiocarcinoma.

Ya-Ping Xu, Ze-Ning Dong, Si-Wei Wang, Yi-Min Zheng, Chi Zhang, Ying-Qun Zhou, Yu-Jie Zhao, Yan Zhao, Feng Wang, Rui Peng and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.7field-weighted citation impact, top 2% of its field
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

37 citing papers in PubMed, 90 citations in OpenAlex.

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  10. The diverse roles of circular RNAs in cholangiocarcinoma.Medical oncology (Northwood, London, England) · 2025
    Review
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  12. Circular RNAs and Cancers.Advances in experimental medicine and biology · 2025
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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 at 5 institutions in 1 country.

Ya-Ping Xu *Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Ze-Ning Dong *Xiangya Medical College, Central South University, Changsha, Hunan, 410008, P. R. China.
Si-Wei Wang *Ministry of Education, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Shanghai, 200032, P. R. China.
Yi-Min Zheng *Ministry of Education, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Shanghai, 200032, P. R. China.
Chi ZhangDepartment of Hepatobiliary and Pancreatic Surgery, Subei People's Hospital, Clinical Medical School, Yangzhou University Affiliated Hospital, Yangzhou, China.
Ying-Qun ZhouDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Yu-Jie ZhaoDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Yan ZhaoDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Feng WangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Rui PengDepartment of Hepatobiliary and Pancreatic Surgery, Subei People's Hospital, Clinical Medical School, Yangzhou University Affiliated Hospital, Yangzhou, China.
Mao-Chun TangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Dou-Sheng BaiDepartment of Hepatobiliary and Pancreatic Surgery, Subei People's Hospital, Clinical Medical School, Yangzhou University Affiliated Hospital, Yangzhou, China. drbaidousheng@126.com.
Xiao-Yong HuangMinistry of Education, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Shanghai, 200032, P. R. China. huang.xiaoyong@zs-hospital.sh.cn.
Chuan-Yong GuoDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China. guochuanyong@hotmail.com.ORCID http://orcid.org/0000-0002-6527-4673
Tongji University · CNFudan University · CNYangzhou University · CNCentral South University · CNNorthern Jiangsu People's Hospital · CN

Funding

fundamental research funds for the central universities 22120180383natural science foundation of shanghai 21ZR1412200
6 · The paper itself

Abstract

backgroundAccumulating evidence indicates that circRNAs may serve as essential regulators in the progression of several human cancers, but the function and mechanism of circRNAs in intrahepatic cholangiocarcinoma (ICC) are largely unknown.

methodsRNA-seq was used to assess differentially expressed circRNAs between 4 ICC and peritumor tissues. Quantitative RT-PCR and in situ hybridization were used to determine the circHMGCS1-016 expression in ICC tissues. The function and mechanism of circHMGCS1-016 were further identified via in vivo experiments. The clinical characteristics and prognostic significance of circHMGCS1-016 were analyzed by a retrospective study. The functions of circHMGCS1-016 were assessed via modifying circRNA expression in ICC cells. Moreover, the molecular mechanisms of circHMGCS1-016 in ICC cells were explored by circRNA precipitation, miRNA immunoprecipitation, SILAC and luciferase reporter assays.

resultsWe identified that compared with peritumor tissues, ICC tissues expressed hsa_circ_0008621 (circHMGCS1-016) high by RNA-seq, which was further identified by qRT-PCR and in situ hybridization. Moreover, the expression of circHMGCS1-016 was revealed to be associated with survival and recurrence of ICC patients. By regulating circHMGCS1-016 expression, we found that elevated circHMGCS1-016 promoted ICC development both in vitro and in vivo. By SILAC and circRNA-pull down, we demonstrated that circHMGCS1-016 induced ICC cell invasion and reshaped the tumor immune microenvironment via the miR-1236-3p/CD73 and GAL-8 axis. In ICC tissues, we uncovered that a high level of circHMGCS1-016 was positively associated with CD73 and GAL-8 expression and negatively related to the CD8

conclusionsCircHMGCS1-016 is a forceful contributor in ICC development and immune tolerance via miR-1236-3p/CD73 and GAL-8 axis. CircHMGCS1-016 can be explored as a new potential biomarker and therapeutic target for PD1-resistant ICC.

Indexed as

RNA, Circular5'-NucleotidaseAnimalsBile Duct NeoplasmsCD8-Positive T-LymphocytesCell Line, TumorCholangiocarcinomaDisease Models, AnimalDisease ProgressionFluorescent Antibody TechniqueGalectinsGene Expression Regulation, NeoplasticGPI-Linked ProteinsHumansHydroxymethylglutaryl-CoA SynthaseImmunohistochemistry5'-NucleotidaseGalectinsGPI-Linked ProteinsHMGCS1 protein, humanHydroxymethylglutaryl-CoA SynthaseMicroRNAsMIRN1236 microRNA, humanNT5E protein, humanRNA, CircularCD73circHMGCS1–016GAL-8Intrahepatic cholangiocarcinomamiR-1236-3p

Identifiers

PMID34526098
PMCPMC8442376
OpenAlexW3201494372

What OpenQuestion holds

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LicenceCC BY
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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.