Evidence map›Paper›PMID 34021267›Full record

ArticleCell death and differentiation2021

YTHDC1-mediated augmentation of miR-30d in repressing pancreatic tumorigenesis via attenuation of RUNX1-induced transcriptional activation of Warburg effect.

Yichao Hou, Qingwei Zhang, Wenjing Pang, Lidan Hou, Yu Liang, Xu Han, Xiaoyu Luo, Ping Wang, Xintian Zhang, Lei Li and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
14.8field-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

123 citing papers in PubMed, 194 citations in OpenAlex.

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  16. mFrontiers in cell and developmental biology · 2026
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63 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

11 authors at 3 institutions in 1 country.

Yichao Hou *Department of Gastroenterology, Shanghai Nineth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Qingwei Zhang *Division of Gastroenterology and Hepatology, Key Laboratory Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Disease, Shanghai, China.
Wenjing Pang *Department of Gastroenterology, Shanghai Nineth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Lidan HouDepartment of Gastroenterology, Shanghai Nineth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yu LiangDepartment of Gastroenterology, Shanghai Nineth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Xu HanDepartment of Gastroenterology, Shanghai Nineth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Xiaoyu LuoDepartment of Gastroenterology, Shanghai Nineth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Ping WangDepartment of Gastroenterology, Shanghai Nineth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Xintian ZhangDepartment of Gastroenterology, Shanghai Nineth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Lei LiDepartment of Gastroenterology, Shanghai Nineth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. lilei2968900@163.com.
Xiangjun MengDepartment of Gastroenterology, Shanghai Nineth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. meng_xiangjun@yahoo.com.
Shanghai Jiao Tong University · CNShanghai Ninth People's Hospital · CNRenji Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) NO. 81802304
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human cancers. It thrives in a malnourished environment; however, little is known about the mechanisms by which PDAC cells actively promote aerobic glycolysis to maintain their metabolic needs. Gene Expression Omnibus (GEO) was used to identify differentially expressed miRNAs. The expression pattern of miR-30d in normal and PDAC tissues was studied by in situ hybridization. The role of miR-30d/RUNX1 in vitro and in vivo was evaluated by CCK8 assay and clonogenic formation as well as transwell experiment, subcutaneous xenograft model and liver metastasis model, respectively. Glucose uptake, ATP and lactate production were tested to study the regulatory effect of miR-30d/RUNX1 on aerobic glycolysis in PDAC cells. Quantitative real-time PCR, western blot, Chip assay, promoter luciferase activity, RIP, MeRIP, and RNA stability assay were used to explore the molecular mechanism of YTHDC1/miR-30d/RUNX1 in PDAC. Here, we discover that miR-30d expression was remarkably decreased in PDAC tissues and associated with good prognosis, contributed to the suppression of tumor growth and metastasis, and attenuation of Warburg effect. Mechanistically, the m

Indexed as

AdenocarcinomaAnimalsCarcinogenesisCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationCore Binding Factor Alpha 2 SubunitFemaleHumansMiceMice, NudeMicroRNAsNerve Tissue ProteinsPrognosisRNA Splicing FactorsWarburg Effect, OncologicCore Binding Factor Alpha 2 SubunitMicroRNAsMirn30d microRNA, mouseNerve Tissue ProteinsRNA Splicing FactorsRunx1 protein, mouseYTHDC1 protein, human

Identifiers

PMID34021267
PMCPMC8563797
OpenAlexW3161215855

What OpenQuestion holds

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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.