Evidence map›Paper›PMID 26305675›Full record

ArticleOncotarget2015

LincRNA-p21 activates endoplasmic reticulum stress and inhibits hepatocellular carcinoma.

Ning Yang, Yong Fu, Haibin Zhang, Hui Sima, Nan Zhu, Guangshun Yang

Abstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–field-weighted citation impact
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

40 citing papers in PubMed.

  1. Review
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  5. Navigating the genomic instability mine field of osteosarcoma to better understand implications of non-coding RNAs.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2022
    Article
  6. Review
  7. Tubule-specific deletion ofMolecular therapy. Nucleic acids · 2021
    Article
  8. Article
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  11. Review
  12. Long intergenic non-coding RNA-p21 is associated with poor prognosis in chronic lymphocytic leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  13. Review
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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.

Ning YangHepatobiliary Surgery Department V, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, China.
Yong FuHepatobiliary Surgery Department V, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, China.
Haibin ZhangHepatobiliary Surgery Department V, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, China.
Hui SimaHepatobiliary Surgery Department V, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, China.
Nan ZhuHepatobiliary Surgery Department V, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, China.
Guangshun YangHepatobiliary Surgery Department V, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LincRNA-p21 is a downstream long non-coding RNA (lncRNA) transcript of p53. LincRNA-p21 serves as a repressor in p53-dependent transcriptional responses and participates in diverse biological processes, including apoptosis, cell cycle, metabolism and pluripotency. However, the role of lincRNA-p21 in human hepatocellular carcinoma remains to be defined. Here in this work, we demonstrated that lincRNA-p21 acted as a tumor suppressive lncRNA in human hepatocellular carcinoma. We firstly found the downregulation of lincRNA-p21 level in human hepatocellular carcinoma tissues, and showed that low expression of lincRNA-p21 was associated with high disease stage and predicted poor survival. Further we showed that lincRNA-p21 knockdown promoted proliferation and colony formation of HepG2, Huh7 and Bel-7042 cells in vitro, while lincRNA-p21 overexpression obtained oppose results. Using tumor xenograft experiments, we also demonstrated that lincRNA-p21 inhibited HepG2 cell growth in vivo and lincRNA-p21 contributed to sorafenib-induced growth regression of HepG2 cell in vivo. Further mechanism analysis revealed that lincRNA-p21 promoted ER stress both in vitro and in vivo, which facilitated apoptosis of hepatocellular carcinoma cells. Finally, we demonstrated that ER stress accounted for lincRNA-p21 effects on apoptosis, proliferation and in vivo growth of hepatocellular carcinoma. These findings implicate that lincRNA-p21 is a potential prognostic factor and therapeutic target for human hepatocellular carcinoma.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBlotting, WesternCarcinoma, HepatocellularCell Line, TumorEndoplasmic Reticulum StressGene Expression Regulation, NeoplasticGene Knockdown TechniquesHep G2 CellsHumansLiver NeoplasmsMaleMice, Inbred BALB CMice, NudeNiacinamideAntineoplastic AgentsNiacinamidePhenylurea CompoundsRNA, Long NoncodingSorafenibER stresshepatocellular carcinomalincRNA-p21sorafenib

Identifiers

PMID26305675
PMCPMC4695050

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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.