Evidence map›Paper›PMID 28476883›Full record

ArticleThe Journal of biological chemistry2017

The long non-coding RNA HOTAIR enhances pancreatic cancer resistance to TNF-related apoptosis-inducing ligand.

Shan-Zhong Yang, Fei Xu, Tong Zhou, Xinyang Zhao, Jay M McDonald, Yabing Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Review
  6. Article
  7. Effect of tumor exosome-derived Lnc RNA HOTAIR on the growth and metastasis of gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
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  15. Article
  16. Noncoding RNAs in apoptosis: identification and function.Turkish journal of biology = Turk biyoloji dergisi · 2022
    Review
  17. Epigenetic regulation of gastrointestinal cancers mediated by long non-coding RNAs.Cancer biomarkers : section A of Disease markers · 2022
    Review
  18. 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

6 authors at 2 institutions in 1 country.

Shan-Zhong YangFrom the Departments of Pathology.
Fei XuFrom the Departments of Pathology.
Tong ZhouMedicine, and.
Xinyang ZhaoBiochemistry, University of Alabama at Birmingham and.
Jay M McDonaldFrom the Departments of Pathology.
Yabing ChenFrom the Departments of Pathology, yabingchen@uabmc.edu.
University of Alabama at Birmingham · USBirmingham VA Medical Center · US

Funding

Death Receptor Signaling in Pancreatic Cancer: Mechanisms and Therapeutic TargetsI01BX002296 · VA · BIRMINGHAM VA MEDICAL CENTER · PI CHEN, YABING · 2014 to 2017
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BLR&D Research Career Scientist Award ApplicationIK6BX003617 · VA · BIRMINGHAM VA MEDICAL CENTER · PI CHEN, YABING · 2017 to 2021
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BLRD VA I01 BX002296BLRD VA IK6 BX003617
6 · The paper itself

Abstract

Pancreatic cancer is a malignant neoplasm with a high mortality rate. Therapeutic agents that activate TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis have shown promising efficacy, but many pancreatic cancers are resistant to TRAIL therapy. Epigenetic regulation plays important roles in tumor pathogenesis and resistance, and a recent study indicated that the long non-coding RNA HOX transcript antisense RNA (HOTAIR) is overexpressed in pancreatic cancer. However, the role of HOTAIR in pancreatic cancer resistance to anticancer agents is unknown. The present study determined the role of HOTAIR in pancreatic cancer TRAIL resistance and investigated the underlying molecular mechanisms. We observed that TRAIL-resistant pancreatic cancer cells had higher levels of HOTAIR expression, whereas TRAIL-sensitive pancreatic cancer cells had lower HOTAIR levels. Overexpressing HOTAIR in TRAIL-sensitive cells attenuated TRAIL-induced apoptosis, and shRNA-mediated HOTAIR knockdown in TRAIL-resistant PANC-1 cells sensitized them to TRAIL-induced apoptosis. These results support a causative effect of HOTAIR on TRAIL sensitivity. Mechanistically, we found that increased HOTAIR expression inhibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increased DR5 expression. We further demonstrated that HOTAIR regulates DR5 expression via the epigenetic regulator enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimethylation on the

Indexed as

ApoptosisCell Line, TumorDrug Resistance, NeoplasmEnhancer of Zeste Homolog 2 ProteinGene Expression Regulation, NeoplasticHistonesHumansMethylationNeoplasm ProteinsPancreatic NeoplasmsReceptors, TNF-Related Apoptosis-Inducing LigandRNA, Long NoncodingRNA, NeoplasmTNF-Related Apoptosis-Inducing LigandEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistonesHOTAIR long untranslated RNA, humanNeoplasm ProteinsReceptors, TNF-Related Apoptosis-Inducing LigandRNA, Long NoncodingRNA, NeoplasmTNF-Related Apoptosis-Inducing LigandTNFRSF10B protein, humanTNFSF10 protein, humanapoptosisdeath receptor 5DR5histone methylationlong non-coding RNA (long ncRNA, lncRNA)pancreatic cancerTRAIL

Identifiers

PMID28476883
PMCPMC5481552
OpenAlexW2611654661

What OpenQuestion holds

Textmetadata
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.