Evidence map›Paper›PMID 27637083›Full record

ArticleOncotarget2016

Long non-coding RNA CRNDE promotes gallbladder carcinoma carcinogenesis and as a scaffold of DMBT1 and C-IAP1 complexes to activating PI3K-AKT pathway.

Sheng Shen, Han Liu, Yueqi Wang, Jiwen Wang, Xiaolin Ni, Zhilong Ai, Hongtao Pan, Houbao Liu, Yebo Shao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-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

30 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
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  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. PI3K Inhibitors in Cancer: Clinical Implications and Adverse Effects.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. The protective role of DMBT1 in cervical squamous cell carcinoma.The Kaohsiung journal of medical sciences · 2019
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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 4 institutions in 1 country.

Sheng ShenDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Han LiuDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Yueqi WangDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Jiwen WangDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Xiaolin NiDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Zhilong AiDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Hongtao PanDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Houbao LiuDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Yebo ShaoDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
The First Affiliated Hospital, Sun Yat-sen University · CNZhongshan Hospital · CNSun Yat-sen University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deleted in malignant brain tumors 1 (DMBT1) is deleted during cancer progression and as a potential tumor-suppressor gene in various types of cancer. However, its role in Gallbladder cancer remains poorly understood. DMBT1 has low-expression and deletion of copy number were detected in normal tissues and GBC cancer tissues by qRT-PCR. Knockdown of DMBT1 increased migration and invasion and overexpressed DMBT1 impaired migration and invasion in GBC cells. We also evaluated the molecular mechanism of DMBT1 by RNA sequencing and GSEA analysis. RNA-Pulldown and RIP assay authenticated CRNDE can specified binding with DMBT1 and c-IAP1. Downregulation of DMBT1 resulted in significant change of gene expression (at least 2-fold) in PI3K-AKT pathway, increased expression of MMP-9, JUK-1, ERK and AKT, activating PI3K-AKT pathway lead to GBC carcinogenesis.We for the first time reported, DMBT1 as a prognosis biomarker, is low-expressed in GBC tumors, and CRNDE act as a scaffold to recruit the DMBT1 and c-IAP1, promotes the PI3K-AKT pathway. Our study reveals DMBT1 may be an important contributor to GBC cancer development.

Indexed as

AnimalsCalcium-Binding ProteinsCell Line, TumorCell MovementCell Transformation, NeoplasticDNA-Binding ProteinsGallbladder NeoplasmsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansInhibitor of Apoptosis ProteinsMaleMicePhosphatidylinositol 3-KinasesPrognosisProtein BindingCalcium-Binding ProteinsCRNDE RNA, humanDMBT1 protein, humanDNA-Binding ProteinsInhibitor of Apoptosis ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Cell SurfaceRNA, Long NoncodingTumor Suppressor Proteinsc-IAP1CRNDEdeleted in malignant brain tumors 1 (DMBT1)GBC carcinogenesismigration and invasion

Identifiers

PMID27637083
PMCPMC5341947
OpenAlexW2518664370

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.