Evidence map›Paper›PMID 28410209›Full record

ArticleOncotarget2017

MiR-106b inhibitors sensitize TRAIL-induced apoptosis in hepatocellular carcinoma through increase of death receptor 4.

Changlong Xu, Liang Shi, Weilai Chen, Peipei Fang, Jie Li, Lingxiang Jin, Zhenzhen Pan, Chenwei Pan

Abstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Role of microRNA-494 in tumor progression.American journal of translational research · 2023
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. The Role of MicroRNAs in Mitochondria-Mediated Eye Diseases.Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. 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

8 authors.

Changlong XuDepartment of Gastroenterology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China.
Liang ShiDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Weilai ChenDepartment of Neurology, Wenzhou People's Hospital, Wenzhou 325027, China.
Peipei FangDepartment of Infectious Disease, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China.
Jie LiDepartment of Infectious Disease, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China.
Lingxiang JinDepartment of Infectious Disease, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China.
Zhenzhen PanDepartment of Infectious Disease, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Chenwei PanDepartment of Infectious Disease, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TNF-related apoptosis-inducing ligand (TRAIL), which is a member of the TNF superfamily, can induce tumor cell apoptosis. However, multiple types of tumor, including hepatocellular carcinoma, show tolerance to TRAIL. Previous studies have demonstrated that tumor cells usually change their expression profile of microRNA (miRNA) to obtain the ability of tolerance to drugs. However, whether such change of miRNA on TRAIL sensitivity is seen in hepatocellular carcinoma still needs to be explored. In this study, we observed overexpression of miR-106b in both HCC patients' tumor tissues and cell lines. Furthermore, we found that overexpression of miR-106b is associated with the sensitivity of TRAIL to HCC. Silencing of miR-106b with antisense oligonucleotide (anti-miR-106b) is proved to enhance the TRAIL-induced apoptosis and reduce the acquired drug resistance to TRAIL in HCC. Mechanically, we didn't observe the obvious change of pro-apoptotic proteins (Bax and Bid) and anti-apoptotic proteins (Bcl-2, Mcl-1 and Bcl-xl) after treatment of anti-miR-106b. However, we used the methods of bioinformatics, flow cytometry, cellular and molecular methods to prove that miR-106b directly targeted to death receptor 4 (DR4) 3'-UTR (3'-Untranslated Regions). MiR-106b inhibitors induced increase of DR4 expression and therefore enhancing TRAIL-mediated apoptosis in HCC. In summary, these results suggest the application of miR-106b inhibitors in HCC treatment. Combination with miR-106b inhibitors and TRAIL may be a novel clinical treatment method on HCC treatment in the future.

Indexed as

3' Untranslated RegionsAnimalsApoptosisCarcinoma, HepatocellularCell Line, TumorDisease Models, AnimalDrug Resistance, NeoplasmGene ExpressionHeterograftsHumansLiver NeoplasmsMiceMicroRNAsReceptors, TNF-Related Apoptosis-Inducing LigandSignal TransductionTNF-Related Apoptosis-Inducing Ligand3' Untranslated RegionsMicroRNAsMIRN106 microRNA, humanReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing Ligandanti-miR-106bapoptosisDR4HCCTRAIL

Identifiers

PMID28410209
PMCPMC5522038

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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.