Evidence map›Paper›PMID 27492460›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

MicroRNA-137 represses FBI-1 to inhibit proliferation and in vitro invasion and migration of hepatocellular carcinoma cells.

Min Zhu, Mingyang Li, Tao Wang, Enqiang Linghu, Benyan Wu

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Bioinformatic analysis andAnnals of translational medicine · 2020
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  7. Review
  8. Article
  9. Review
  10. Article
  11. FBI-1 mRNA in normal mucosa is an independent prognostic factor in colorectal cancer patients.International journal of clinical and experimental pathology · 2018
    Article
  12. Article
  13. 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

5 authors at 2 institutions in 1 country.

Min ZhuDepartment of Oncology, Nan Lou Division, Chinese PLA General Hospital, Beijing, 100853, China.
Mingyang LiDepartment of Gastroenterology, Chinese PLA General Hospital, Beijing, 100853, China.
Tao WangInstitute of Toxicology and Pharmacology, Chinese Military Medical Science Academy, Beijing, 100850, China.
Enqiang LinghuDepartment of Gastroenterology, Chinese PLA General Hospital, Beijing, 100853, China.
Benyan WuDepartment of Gastroenterology, Nan Lou Division, Chinese PLA General Hospital, Beijing, 100853, China. benyanwu@vip.sina.com.
Chinese PLA General Hospital · CNAcademy of Military Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pro-oncogene factor that binds to inducer of short transcripts-1 (FBI-1), which is encoded by ZBTB7A gene and belongs to POK (POZ/BTB and KrÜppel) protein family, has been shown to enhance hepatocellular carcinoma (HCC) cells proliferation and multi-drug resistance (MDR) process. However, the possibility that FBI-1 is a therapeutic target for further HCC treatment remains poorly determined. In the current study, two microRNA (miRNA) target prediction programs (TargetScan and MiRanda) were used to identify miR-137 as a potential regulator of FBI-1. Our results showed that expression of miR-137 was downregulated, while FBI-1 was upregulated in clinical HCC specimens, compared with paired non-tumor specimens. Overexpression of miR-137 via adenoviral vector inhibited the proliferation and anchorage-independent growth of HCC cells, HepG2 and MHCC-97H. Our data also showed that miR-137 repressed endogenous expression level of FBI-1, as well as Notch-1 and Survivin. MiR-137 also inhibited in vitro invasion and migration of HCC cells and attenuated their epithelial-mesenchymal transition (EMT) process. Moreover, miR-137 suppressed the growth rate of HepG2 cells in nude mice model. Overexpression of miR-137 via its adenoviral vector enhanced the sensitivity of HepG2 cells to anti-tumor drugs and attenuated the MDR process of a resistance cell line HepG2/adriamycin (ADR). Thus, FBI-1 downregulation mediated by miR-137 overexpression may be a potential strategy for HCC treatment.

Indexed as

Cell MovementCell ProliferationAnimalsApoptosisBiomarkers, TumorBlotting, WesternCarcinoma, HepatocellularDNA-Binding ProteinsEpithelial-Mesenchymal TransitionFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansImmunoenzyme TechniquesLiver NeoplasmsMaleBiomarkers, TumorDNA-Binding ProteinsMicroRNAsMIRN137 microRNA, humanRNA, MessengerTranscription FactorsZBTB7A protein, humanFBI-1HCCInvasion and migrationmiR-137Multi-drug resistance

Identifiers

PMID27492460
OpenAlexW2485498491

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.