Evidence map›Paper›PMID 31372043›Full record

ArticleCancer management and research2019

DNMT3a promotes proliferation by activating the STAT3 signaling pathway and depressing apoptosis in pancreatic cancer.

Wei Jing, Na Song, Yun-Peng Liu, Xiu-Juan Qu, Ya-Fei Qi, Ce Li, Ke-Zuo Hou, Xiao-Fang Che, Xiang-Hong Yang

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  7. Life science alliance · 2023
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  14. BioMed research international · 2020
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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

9 authors at 2 institutions in 1 country.

Wei JingThe First Department of Oncology, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.
Na SongDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, People's Republic of China.
Yun-Peng LiuDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, People's Republic of China.
Xiu-Juan QuDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, People's Republic of China.
Ya-Fei QiDepartment of Pathology, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.
Ce LiDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, People's Republic of China.
Ke-Zuo HouDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, People's Republic of China.
Xiao-Fang CheDepartment of Medical Oncology, The First Hospital of China Medical University, Shenyang, People's Republic of China.
Xiang-Hong YangDepartment of Pathology, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.
First Hospital of China Medical University · CNChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough aberrant DNA methyltransferase 3a (DNMT3a) expression is important to the tumorigenesis of pancreatic ductal adenocarcinoma (PDAC), the role of DNMT3a in PDAC prognosis is not clarified yet due to the limited studies and lacking of underlying molecular mechanism.

methodsThe expression of DNMT3a was examined by immunohistochemistry in PDAC tissues. Gene expression profiles assays were conducted to explore the impact of DNMT3a on biological processes and signal pathways. Cell cycle and apoptosis were measured by flow cytometry. Western blotting and real-time qPCR assays were used to explore the impact of DNMT3a on expression of protein and mRNA related to cell cycle, STAT3 signaling pathway and apoptosis.

resultsDNMT3a was overexpressed and closely associated with poor outcomes of PDAC. DNMT3a knockdown restrained PDAC cell proliferation, induced cell cycle arrest and promoted apoptosis in vitro. Affymetrix GeneChip Human Transcriptome Array identified that the cell cycle-related process was most significantly associated with DNMT3a. DNMT3a knockdown induced G1-S phase transition arrest by decreasing the expression of cyclin D1, which was mediated by the reduction of IL8 and the subsequent inactivation of STAT3 signaling pathway. Furthermore, exogenous apoptosis was also promoted after DNMT3a knockdown, probably via up-regulation of DNA transcription and expression in CASP8.

conclusionThese findings indicate that DNMT3a plays an important role in PDAC progression. DNMT3a may serve as a prognostic biomarker and a therapeutic strategy candidate in PDAC.

Indexed as

DNA methyltransferase 3apancreatic ductal adenocarcinomaprognosisproliferation

Identifiers

PMID31372043
PMCPMC6635825
OpenAlexW2956518497

What OpenQuestion holds

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LicenceCC BY-NC
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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.