Evidence map›Paper›PMID 31616182›Full record

ArticleCancer management and research2019

BHLHE41 promotes U87 and U251 cell proliferation via ERK/cyclinD1 signaling pathway.

Chen Wang, Na Zhao, Qin Zheng, Di Zhang, Yang Liu

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Approach to Functions ofInternational journal of molecular sciences · 2023
    Review
  6. Article
  7. The BRCT Domain from the Homologue of the Oncogene PES1 inInternational journal of molecular sciences · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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.

Chen WangDepartment of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang 110122, People's Republic of China.
Na ZhaoDepartment of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang 110122, People's Republic of China.
Qin ZhengDepartment of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang 110122, People's Republic of China.
Di ZhangDepartment of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang 110122, People's Republic of China.
Yang LiuDepartment of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang 110122, People's Republic of China.
First Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe biological functions of BHLHE41 in the proliferation of glioblastoma remained unexplored. We aimed to investigate the biological roles and underlying molecular mechanisms of BHLHE41 in glioblastoma. MATERIALS AND

methodsWe used multiple methods, including Western blot analysis, soft agar colony-formation assay, CCK8 assay, and flow cytometry, to evaluate the changes in multiple cellular functions after BHLHE41 knockdown or overexpression in U87 and U251 cell lines. The TCGA database was then used to analyze the associations between BHLHE41 expression with clinicopathological factors and the overall survival (OS) of glioma patients.

resultsThis study determined that overexpression of BHLHE41 promoted glioma cell proliferation and colony formation. Besides, BHLHE41 upregulated cyclinD1, cyclinD3, and cyclinE1 expression and drove phase transition from G1 to S and G2 phases by upregulating these cyclins. In contrast, knockdown of BHLHE41 had an opposite effect on all of these parameters. However, BHLHE41 had no effect on apoptosis. Moreover, BHLHE41 activated MAPK/ERK signaling pathway to upregulate cyclinD1 expression. After the ERK signal pathway was blocked by a specific inhibitor, SCH772984, cyclinD1 upregulation was reversed. Furthermore, the median OS of low-grade glioma (LGG) patients with low to median level of BHLHE41 was 22.6 months, longer than that of the patients with high level of BHLHE41 (21.0 months).

conclusionBHLHE41 has an important role in the proliferation of glioblastoma and could serve as a novel candidate for targeted therapy of glioblastoma.

Indexed as

BHLHE41cell cyclecyclinD1ERKglioblastomaproliferation

Identifiers

PMID31616182
PMCPMC6698591
OpenAlexW2967254148

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.