Evidence map›Paper›PMID 26741116›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2016

Expression of Tim4 in Glioma and its Regulatory Role in LN-18 Glioma Cells.

Weiguo Li, Xingang Li, Shujun Xu, Xiangyu Ma, Qiujie Zhang

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Tim-4 in Health and Disease: Friend or Foe?Frontiers in immunology · 2020
    Review
  8. Downregulation of TBC1 Domain Family Member 24 (BC1D24) Inhibits Breast Carcinoma Growth via IGF1R/PI3K/AKT Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  9. Article
  10. SHP-2 Activating Mutation Promotes Malignant Biological Behaviors of Glioma Cells.Medical science monitor : international medical journal of experimental and clinical research · 2017
    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 1 institution in 1 country.

Weiguo LiDepartment of Neurosurgery, Qilu Hospital, Shandong University, Jinan, Shandong, China (mainland).
Xingang LiDepartment of Neurosurgery, Qilu Hospital, Shandong University, Jinan, Shandong, China (mainland).
Shujun XuDepartment of Neurosurgery, Qilu Hospital, Shandong University, Jinan, Shandong, China (mainland).
Xiangyu MaDepartment of Neurosurgery, Qilu Hospital, Shandong University, Jinan, Shandong, China (mainland).
Qiujie ZhangDepartment of Health, Qilu Hospital, Shandong University, Jinan, Shandong, China (mainland).
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTim4 is a transmembrane protein known as T cell immunoglobulin and mucin domain containing protein-4. We speculated that Tim4 might be associated with glioma. This study aimed to investigate the expression level of Tim4 in gliomas and the regulatory role of Tim4 on the growth and apoptosis of LN-18 glioma cells. MATERIAL/

methodsTumor tissues and adjacent normal tissues were collected from patients with glioma. The expression level of Tim4 mRNA and protein was determined by RT-PCR and Western blot analyses, respectively to evaluate their association with glioma. Tim4 was overexpressed or silenced by siRNA interference in cultured human glioma cells LN-18. The growth and apoptosis of LN-18 cells was detected by MTT assay and flow cytometry. The colony-forming ability of LN-18 cells was assessed by the colony formation assay. The collection of human tissues was approved by the Research Ethics Committee at the Harbin Medical University Cancer Hospital and performed in strict accordance with international standards. All patients were required to sign the informed consent.

resultsThe expression level of Tim4 mRNA and protein in tumor tissues was significantly higher compared with adjacent normal tissues. Antisense miRNA targeting Tim4 inhibited the growth of LN-18 cells, induced their apoptosis, and reduced their clonogenic capacity. In contrast, overexpression of Tim4 promoted the growth of LN-18 cells, inhibited their apoptosis, and enhanced their clonogenic potential.

conclusionsThe expression level of Tim-4 is closely associated with glioma. Decreased expression of Tim4 inhibited the growth and colony-forming ability of LN-18 cells and induced their apoptosis, whereas increased expression of Tim4 stimulated the growth and clonogenic potential of LN-18 cells and suppressed their apoptosis.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBrain NeoplasmsCaspase 3Cell Line, TumorFlow CytometryGene Expression ProfilingGliomaHumansMembrane ProteinsRNA InterferenceRNA, MessengerRNA, Small InterferingCASP3 protein, humanCaspase 3Membrane ProteinsRNA, MessengerRNA, Small InterferingTIMD4 protein, human

Identifiers

PMID26741116
PMCPMC4710195
OpenAlexW2232445521

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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.