Evidence map›Paper›PMID 26542803›Full record

ArticleThe Journal of biological chemistry2016

MicroRNA-7 Compromises p53 Protein-dependent Apoptosis by Controlling the Expression of the Chromatin Remodeling Factor SMARCD1.

Chun-Fu Hong, Shu-Yu Lin, Yu-Ting Chou, Cheng-Wen Wu

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Noncoding RNAs in apoptosis: identification and function.Turkish journal of biology = Turk biyoloji dergisi · 2022
    Review
  9. Article
  10. MiR-7 in Cancer Development.Biomedicines · 2021
    Review
  11. Role of microRNA-7 in liver diseases: a comprehensive review of the mechanisms and therapeutic applications.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2020
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. MicroRNAs, DNA Damage Response, and Cancer Treatment.International journal of molecular sciences · 2016
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 4 institutions in 3 countries.

Chun-Fu HongFrom the Department of Long Term Care, National Quemoy University, Kinmen County 89250.
Shu-Yu Linthe National Research Program for Genomic Medicine Core Facilities for Proteomics and Glycomics, Institute of Biological Chemistry, Academia Sinica, Taipei 11529.
Yu-Ting Chouthe Institute of Biotechnology, National Tsing Hua University, HsinChu 30013,. Electronic address: ytchou@life.nthu.edu.tw.
Cheng-Wen Wuthe Institute of Clinical Medicine,; Institute of Biochemistry and Molecular Biology, and; Institute of Microbiology and Immunology, National Yang Ming University, Taipei 11221, and; the Institute of Biomedical Science, Academia Sinica, Taipei 11221, Taiwan. Electronic address: cwwu@ym.edu.tw.
Czech Academy of Sciences, Institute of Microbiology · CZInstitute of Biological Chemistry, Academia Sinica · TWNational Quemoy University · TWNational Tsing Hua University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously demonstrated that the epidermal growth factor receptor (EGFR) up-regulated miR-7 to promote tumor growth during lung cancer oncogenesis. Several lines of evidence have suggested that alterations in chromatin remodeling components contribute to cancer initiation and progression. In this study, we identified SMARCD1 (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily d, member 1) as a novel target gene of miR-7. miR-7 expression reduced SMARCD1 protein expression in lung cancer cell lines. We used luciferase reporters carrying wild type or mutated 3'UTR of SMARCD1 and found that miR-7 blocked SMARCD1 expression by binding to two seed regions in the 3'UTR of SMARCD1 and down-regulated SMARCD1 mRNA expression. Additionally, upon chemotherapy drug treatment, miR-7 down-regulated p53-dependent apoptosis-related gene BAX (BCL2-associated X protein) and p21 expression by interfering with the interaction between SMARCD1 and p53, thereby reducing caspase3 cleavage and the downstream apoptosis cascades. We found that although SMARCD1 sensitized lung cancer cells to chemotherapy drug-induced apoptosis, miR-7 enhanced the drug resistance potential of lung cancer cells against chemotherapy drugs. SMARCD1 was down-regulated in patients with non-small cell lung cancer and lung adenocarcinoma cell lines, and SMARCD1 and miR-7 expression levels were negatively correlated in clinical samples. Our investigation into the involvement of the EGFR-regulated microRNA pathway in the SWI/SNF chromatin remodeling complex suggests that EGFR-mediated miR-7 suppresses the coupling of the chromatin remodeling factor SMARCD1 with p53, resulting in increased chemo-resistance of lung cancer cells.

Indexed as

ApoptosisGene Expression RegulationCell Line, TumorChromatinChromosomal Proteins, Non-HistoneGene Expression Regulation, NeoplasticHumansLung NeoplasmsMicroRNAsProtein BindingTranscription FactorsTumor Suppressor Protein p53ChromatinChromosomal Proteins, Non-HistoneMicroRNAsMIRN7-1 microRNA, humanSMARCD1 protein, humanTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53drug resistanceepidermal growth factor receptor (EGFR)lung cancermicroRNA (miRNA)p53SMARCD1

Identifiers

PMID26542803
PMCPMC4722465
OpenAlexW2166904216

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.