Evidence map›Paper›PMID 30158112›Full record

ArticleThe EMBO journal2018

Function of HNRNPC in breast cancer cells by controlling the dsRNA-induced interferon response.

Yusheng Wu, Wenwei Zhao, Yang Liu, Xiangtian Tan, Xin Li, Qin Zou, Zhengtao Xiao, Hui Xu, Yuting Wang, Xuerui Yang

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

128 citing papers in PubMed, 1 synthesis or guideline pooled it, 197 citations in OpenAlex.

  1. Pooled it
  2. YBX1 regulates RNA polymerase III transcripts to prevent inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Review
  5. HnRNP C binding to invertedScience advances · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. mFrontiers in cell and developmental biology · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

68 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Yusheng WuTsinghua-Peking Joint Center for Life Sciences, Beijing, China.
Wenwei ZhaoMOE Key Laboratory of Bioinformatics, Tsinghua University, Beijing, China.
Yang LiuMOE Key Laboratory of Bioinformatics, Tsinghua University, Beijing, China.
Xiangtian TanMOE Key Laboratory of Bioinformatics, Tsinghua University, Beijing, China.
Xin LiMOE Key Laboratory of Bioinformatics, Tsinghua University, Beijing, China.
Qin ZouMOE Key Laboratory of Bioinformatics, Tsinghua University, Beijing, China.
Zhengtao XiaoTsinghua-Peking Joint Center for Life Sciences, Beijing, China.
Hui XuTsinghua-Peking Joint Center for Life Sciences, Beijing, China.
Yuting WangMOE Key Laboratory of Bioinformatics, Tsinghua University, Beijing, China.
Xuerui YangTsinghua-Peking Joint Center for Life Sciences, Beijing, China yangxuerui@tsinghua.edu.cn.ORCID 0000-0002-7731-2147
Center for Life Sciences · CNNational Institute of Biological Sciences, Beijing · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated expression of RNA binding protein HNRNPC has been reported in cancer cells, while the essentialness and functions of HNRNPC in tumors were not clear. We showed that repression of HNRNPC in the breast cancer cells MCF7 and T47D inhibited cell proliferation and tumor growth. Our computational inference of the key pathways and extensive experimental investigations revealed that the cascade of interferon responses mediated by RIG-I was responsible for such tumor-inhibitory effect. Interestingly, repression of HNRNPC resulted in accumulation of endogenous double-stranded RNA (dsRNA), the binding ligand of RIG-I. These up-regulated dsRNA species were highly enriched by Alu sequences and mostly originated from pre-mRNA introns that harbor the known HNRNPC binding sites. Such source of dsRNA is different than the recently well-characterized endogenous retroviruses that encode dsRNA In summary, essentialness of HNRNPC in the breast cancer cells was attributed to its function in controlling the endogenous dsRNA and the down-stream interferon response. This is a novel extension from the previous understandings about HNRNPC in binding with introns and regulating RNA splicing.

Indexed as

Gene Expression Regulation, NeoplasticUp-RegulationAnimalsBreast NeoplasmsFemaleHeterogeneous-Nuclear Ribonucleoprotein Group CHumansInterferonsIntronsMCF-7 CellsMiceNeoplasm ProteinsRNA, Double-StrandedRNA, NeoplasmRNA SplicingUbiquitin-Protein LigasesHeterogeneous-Nuclear Ribonucleoprotein Group CHNRNPC protein, humanInterferonsNeoplasm ProteinsRNA, Double-StrandedRNA, NeoplasmRNF135 protein, humanUbiquitin-Protein Ligasesbreast cancerdouble‐stranded RNAHNRNPCinterferon responseinterferon signalingMCF7T47Dtumorigenesis

Identifiers

PMID30158112
PMCPMC6276880
OpenAlexW2889210641

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.