Evidence map›Paper›PMID 36068586›Full record

ArticleJournal of hematology & oncology2022

Hypoxia-induced exosomal circPDK1 promotes pancreatic cancer glycolysis via c-myc activation by modulating miR-628-3p/BPTF axis and degrading BIN1.

Jiewei Lin, Xinjing Wang, Shuyu Zhai, Minmin Shi, Chenghong Peng, Xiaxing Deng, Da Fu, Jiancheng Wang, Baiyong Shen

Open access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
14.1field-weighted citation impact, top 1% 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

116 citing papers in PubMed, 167 citations in OpenAlex.

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56 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Jiewei Lin *Department of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xinjing Wang *Department of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shuyu Zhai *Department of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Minmin ShiResearch Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chenghong PengDepartment of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaxing DengDepartment of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Da FuResearch Institute of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China. fuda@shsmu.edu.cn.
Jiancheng WangDepartment of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. jiancheng_wang@hotmail.com.
Baiyong ShenDepartment of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. shenby@shsmu.edu.cn.
Shanghai Jiao Tong University · CNRuijin Hospital · CN

Funding

Medical- Engineering Cross Foundation of Shanghai Jiao Tong University ZH2018ZDA01National Nature Science Foundation of China 81802358National Nature Science Foundation of China 81871906Translational Medicine Program of Major National Science and Technology Infrastructure TMSK-2021-507
6 · The paper itself

Abstract

backgroundcircRNA has been established to play a pivotal role in tumorigenesis development in a variety of cancers; nevertheless, the biological functions and molecular mechanisms of hypoxia-induced exosomal circRNAs in pancreatic cancer remain largely unknown.

methodsDifferentially expressed circRNAs in exosomes between hypoxic exosomes and normoxic exosomes in PC cells were verified by RNA sequencing. The expression of circPDK1 in PC tumors and PC patients was evaluated by qRT-PCR and ISH, and the biological functions of circPDK1 in PC were verified through a series of in vitro and in vivo experiments. Using Western blotting, Co-IP, RNA pull-down, ChIP, RIP, dual-luciferase assays, and rescue experiments, the underlying mechanism of circPDK1 was verified.

resultsCircPDK1 was highly abundant in PC tumor tissues and serum exosomes and was associated with poor survival. Exosomal circPDK1 significantly promoted PC cell proliferation, migration, and glycolysis both in vitro and in vivo. Mechanistically, circPDK1 could be activated by HIF1A at the transcriptional level and sponges miR-628-3p to activate the BPTF/c-myc axis. In addition, circPDK1 serves as a scaffold that enhances the interaction between UBE2O and BIN1, inducing the UBE2O-mediated degradation of BIN1.

conclusionsWe found that circPDK1 was activated by HIF1A at the transcriptional level by modulating the miR-628-3p/BPTF axis and degrading BIN1. Exosomal circPDK1 is a promising biomarker for PC diagnosis and prognosis and represents a potential therapeutic target for PC.

Indexed as

ExosomesMicroRNAsPancreatic NeoplasmsAdaptor Proteins, Signal TransducingCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGlycolysisHumansHypoxiaNuclear ProteinsRNA, CircularTumor Suppressor ProteinsUbiquitin-Conjugating EnzymesAdaptor Proteins, Signal TransducingBIN1 protein, humanMicroRNAsMIRN628 microRNA, humanNuclear ProteinsRNA, CircularTumor Suppressor ProteinsUBE2O protein, humanUbiquitin-Conjugating EnzymesceRNAcircRNAExosomesHypoxiaPancreatic cancerUbiquitination

Identifiers

PMID36068586
PMCPMC9450374
OpenAlexW4294842401

What OpenQuestion 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 OpenQuestion graph.