Evidence map›Paper›PMID 38012734›Full record

ArticleJournal of experimental & clinical cancer research : CR2023

Extracellular vesicle-packaged circBIRC6 from cancer-associated fibroblasts induce platinum resistance via SUMOylation modulation in pancreatic cancer.

Shangyou Zheng, Qing Tian, Yuan Yuan, Shuxin Sun, Tingting Li, Renpeng Xia, Rihua He, Yuming Luo, Qing Lin, Zhiqiang Fu and 3 more

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

Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 39 citations in OpenAlex.

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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

13 authors at 6 institutions in 1 country.

Shangyou Zheng *Department of Pancreas Center, Department of General Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, Guangdong, China.
Qing Tian *School of medicine, South China University of Technology, Guangzhou, 510006, Guangdong Province, China.
Yuan Yuan *Guangdong cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, Guangdong, China.
Shuxin Sun *Department of Pancreas Center, Department of General Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, Guangdong, China.
Tingting LiSchool of medicine, South China University of Technology, Guangzhou, 510006, Guangdong Province, China.
Renpeng XiaThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Rihua HeDepartment of Pancreas Center, Department of General Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, Guangdong, China.
Yuming LuoDepartment of Pancreas Center, Department of General Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, Guangdong, China.
Qing LinDepartment of Pancreas Center, Department of General Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, Guangdong, China.
Zhiqiang FuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, Guangdong, China.
Yu ZhouDepartment of Pancreas Center, Department of General Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, Guangdong, China. zhouyu@gdph.org.cn.
Rufu ChenDepartment of Pancreas Center, Department of General Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, Guangdong, China. chenrufu@gdph.org.cn.
Chonghui HuDepartment of Pancreas Center, Department of General Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, Guangdong, China. huchonghui@gdph.org.cn.ORCID http://orcid.org/0000-0001-9305-9834
Guangdong Academy of Medical Sciences · CNGuangdong General Hospital · CNSouth China University of Technology · CNShantou University · CNSouthern Medical University · CNSun Yat-sen University · CN

Funding

Guangdong Science and Technology Department 2021A1515011089National Key Clinical Specialty Discipline Construction Program of China 2022YW030009National Natural Science Foundation of China 82072639National Natural Science Foundation of China 82203599National Natural Science Foundation of China 82203691National Natural Science Foundation of China 82372859
6 · The paper itself

Abstract

backgroundCancer-associated fibroblasts (CAFs) play pivotal roles in chemoresistance of pancreatic ductal adenocarcinoma (PDAC). However, the underlying mechanisms are poorly understood. Revealing the cross-talk network between tumor stroma and pancreatic cancer and developing effective strategies against oxaliplatin resistance are highly desired in the clinic.

methodsHigh-throughput sequence was used to screened the key circRNAs transmitted by extracellular vesicles (EVs) from CAFs to pancreatic cancer cells. The associations between EV-packaged circBIRC6 and chemotherapy responsiveness were validated in a cohort of 82 cases of advanced PDAC patients. Then, the effects of EV-packaged circBIRC6 on CAF-induced oxaliplatin resistance were investigated by flow cytometry, colony formation, viability of pancreatic cancer organoids in vitro and by xenograft models in vivo. RNA pulldown, RNA immunoprecipitation, and sites mutation assays were used to reveal the underlying mechanism.

resultsWe identified a circRNA, circBIRC6, is significantly upregulated in CAF-derived EVs and is positively associated with oxaliplatin-based chemoresistance. In vitro and in vivo functional assays showed that CAF-derived EV-packaged circBIRC6 enhance oxaliplatin resistance of pancreatic cancer cells and organoids via regulating the non-homologous end joining (NHEJ) dependent DNA repair. Mechanistically, circBIRC6 directly binds with XRCC4 and enhanced the interaction of XRCC4 with SUMO1 at the lysine 115 residue, which facilitated XRCC4 chromatin localization. XRCC4

conclusionsOur study revealed that EV-packaged circBIRC6 confer oxaliplatin resistance in PDAC by mediating SUMOylation of XRCC4, introducing a promising predictive and therapeutic target for PDAC on oxaliplatin resistance.

Indexed as

Cancer-Associated FibroblastsCarcinoma, Pancreatic DuctalExtracellular VesiclesPancreatic NeoplasmsHumansOxaliplatinPlatinumRNASumoylationOxaliplatinPlatinumRNACancer-associated fibroblastsCircular RNAsExtracellular vesiclesNon-homologous end joiningOxaliplatin resistance.SUMOylation

Identifiers

PMID38012734
PMCPMC10683239
OpenAlexW4389098916

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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.