Evidence map›Paper›PMID 31391552›Full record

ArticleOncogene2019

LINC00346 promotes pancreatic cancer progression through the CTCF-mediated Myc transcription.

Wan-Xin Peng, Rong-Zhang He, Ziqiang Zhang, Liu Yang, Yin-Yuan Mo

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. Article
  9. Target c-Myc to treat pancreatic cancer.Cancer biology & therapy · 2022
    Article
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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

5 authors at 4 institutions in 2 countries.

Wan-Xin PengKey Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China.
Rong-Zhang HeCancer Institute, University of Mississippi Medical Center, Jackson, MS, USA.
Ziqiang ZhangDepartment of Pulmonary Medicine, Tongji Hospital, Tongji University, Shanghai, 200065, China.
Liu YangKey Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, 310014, China. yangliuqq2003@163.com.
Yin-Yuan MoCancer Institute, University of Mississippi Medical Center, Jackson, MS, USA. ymo@umc.edu.
University of Mississippi Medical Center · USHangzhou Medical College · CNTongji Hospital · CNZhejiang Provincial People's Hospital · CN

Funding

The Akt-associated microRNAs in cancer cellsR01CA154989 · NCI · UNIVERSITY OF MISSISSIPPI MED CTR · PI MO, YIN-YUAN · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA154989
6 · The paper itself

Abstract

Although multiple factors are known to contribute to pancreatic ductal adenocarcinoma (PDAC) progression, the role of long non-coding RNAs (lncRNAs) in PDAC remains largely unknown. In this study, we present data that long intergenic non-coding RNA 346 (LINC00346) functions as a promoting factor for PDAC development. We first show that LINC00346 is highly expressed in pancreatic tumor specimens as compared to normal pancreatic tissue based on interrogation of The Cancer Genome Atlas (TCGA) pancreatic adenocarcinoma dataset. Of significance, this upregulation of LINC00346 is associated with overall survival (OS) and disease-free survival (DFS), respectively. We further show that knockout (KO) of LINC00346 impairs pancreatic cancer cell proliferation, tumorigenesis, migration, and invasion ability. Importantly, these phenotypes can be restored by LINC00346 re-expression in KO cells (i.e., rescue experiment). RNA precipitation assays combined with mass spectrometry analysis indicate that LINC00346 interacts with CCCTC-binding factor (CTCF), a known transcriptional repressor of c-Myc. This interaction between LINC00346 and CTCF prevents the binding of CTCF to c-Myc promoter, relieving the CTCF-mediated repression of c-Myc. Thus, LINC00346 functions as a positive transcriptional regulator of c-Myc. Together, these results suggest that LINC00346 contributes to PDAC pathogenesis by activating c-Myc, and as such, LINC00346 may serve as a potential biomarker and therapeutic target for PDAC.

Indexed as

Transcription, GeneticBiomarkers, TumorCarcinoma, Pancreatic DuctalCCCTC-Binding FactorCell ProliferationDisease ProgressionHumansNeoplasm InvasivenessNeoplasm MetastasisPancreatic NeoplasmsPrognosisPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-mycRNA, Long NoncodingBiomarkers, TumorCCCTC-Binding FactorCTCF protein, humanProto-Oncogene Proteins c-mycRNA, Long Noncoding

Identifiers

PMID31391552
OpenAlexW2965128075

What OpenQuestion holds

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Read underepoch 390

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.