Evidence map›Paper›PMID 33849617›Full record

ArticleJournal of hematology & oncology2021

CLK1/SRSF5 pathway induces aberrant exon skipping of METTL14 and Cyclin L2 and promotes growth and metastasis of pancreatic cancer.

Shi Chen, Can Yang, Zu-Wei Wang, Jian-Fei Hu, Jing-Jing Pan, Cheng-Yu Liao, Jia-Qiang Zhang, Jiang-Zhi Chen, Yi Huang, Long Huang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
9.3field-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

84 citing papers in PubMed, 144 citations in OpenAlex.

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24 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

14 authors at 5 institutions in 1 country.

Shi Chen *Shengli Clinical Medical College of Fujian Medical University, Fujian Medical University, No. 134, East Street, Fuzhou, 350001, Fujian Province, People's Republic of China. wawljwalj@163.com.
Can Yang *Shengli Clinical Medical College of Fujian Medical University, Fujian Medical University, No. 134, East Street, Fuzhou, 350001, Fujian Province, People's Republic of China.
Zu-Wei Wang *Shengli Clinical Medical College of Fujian Medical University, Fujian Medical University, No. 134, East Street, Fuzhou, 350001, Fujian Province, People's Republic of China.
Jian-Fei Hu *Shengli Clinical Medical College of Fujian Medical University, Fujian Medical University, No. 134, East Street, Fuzhou, 350001, Fujian Province, People's Republic of China.
Jing-Jing PanShengli Clinical Medical College of Fujian Medical University, Fujian Medical University, No. 134, East Street, Fuzhou, 350001, Fujian Province, People's Republic of China.
Cheng-Yu LiaoShengli Clinical Medical College of Fujian Medical University, Fujian Medical University, No. 134, East Street, Fuzhou, 350001, Fujian Province, People's Republic of China.
Jia-Qiang ZhangDepartment of General Surgery, Pancreatic Disease Center, Research Institute of Pancreatic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, No.197 Ruijin Second Road, Shanghai, 200025, People's Republic of China.
Jiang-Zhi ChenDepartment of Hepatobiliary Surgery, Union Hospital, Fujian Medical University, Fuzhou, 350001, People's Republic of China.
Yi HuangShengli Clinical Medical College of Fujian Medical University, Fujian Medical University, No. 134, East Street, Fuzhou, 350001, Fujian Province, People's Republic of China.
Long HuangShengli Clinical Medical College of Fujian Medical University, Fujian Medical University, No. 134, East Street, Fuzhou, 350001, Fujian Province, People's Republic of China.
Qian ZhanDepartment of General Surgery, Pancreatic Disease Center, Research Institute of Pancreatic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, No.197 Ruijin Second Road, Shanghai, 200025, People's Republic of China.
Yi-Feng TianShengli Clinical Medical College of Fujian Medical University, Fujian Medical University, No. 134, East Street, Fuzhou, 350001, Fujian Province, People's Republic of China.
Bai-Yong ShenDepartment of General Surgery, Pancreatic Disease Center, Research Institute of Pancreatic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, No.197 Ruijin Second Road, Shanghai, 200025, People's Republic of China. shenbaiyongrj@126.com.
Yao-Dong WangShengli Clinical Medical College of Fujian Medical University, Fujian Medical University, No. 134, East Street, Fuzhou, 350001, Fujian Province, People's Republic of China. wangyaodongch@126.com.
Fujian Medical University · CNRuijin Hospital · CNFujian Provincial Hospital · CNFujian Provincial People's Hospital · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBoth aberrant alternative splicing and m6A methylation play complicated roles in the development of pancreatic cancer (PC), while the relationship between these two RNA modifications remains unclear.

methodsRNA sequencing (RNA-seq) was performed using 15 pairs of pancreatic ductal adenocarcinoma (PDAC) tissues and corresponding normal tissues, and Cdc2-like kinases 1 (CLK1) was identified as a significantly upregulated alternative splicing related gene. Real-time quantitative PCR (qPCR) and western blotting were applied to determine the CLK1 levels. The prognostic value of CLK1 was elucidated by Immunohistochemistry (IHC) analyses in two independent PDAC cohorts. The functional characterizations and mechanistic insights of CLK1 in PDAC growth and metastasis were evaluated with PDAC cell lines and nude mice. SR-like splicing factors5

resultsCLK1 expression was significantly increased in PDAC tissues at both the mRNA and protein levels. High CLK1 expression was associated with poor prognosis. Elevated CLK1 expression promoted growth and metastasis of PC cells in vitro and in vivo. Mechanistically, CLK1 enhanced phosphorylation on SRSF5

conclusionsThe CLK1/SRSF5 pathway induces aberrant exon skipping of METTL14 and Cyclin L2, which promotes growth and metastasis and regulates m6A methylation of PDAC cells. This study suggests the potential prognostic value and therapeutic targeting of this pathway in PDAC patients.

Indexed as

ExonsAnimalsBiomarkers, TumorCell Growth ProcessesCell Line, TumorCell MovementCyclinsFemaleHEK293 CellsHeterograftsHumansMaleMethyltransferasesMiceMice, Inbred BALB CMice, NudeBiomarkers, TumorCCNL2 protein, humanClk dual-specificity kinasesCyclinsMethyltransferasesMETTL14 protein, humanProtein Serine-Threonine KinasesProtein-Tyrosine KinasesSerine-Arginine Splicing FactorsSRSF5 protein, humanTranscription FactorsAlternative splicingCLK1Cyclin L2M6A ModificationMETTL14Pancreatic cancerSRSF5

Identifiers

PMID33849617
PMCPMC8045197
OpenAlexW3152757543

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.