Evidence map›Paper›PMID 31388332›Full record

ArticleCancer cell international2019

miR-450b-5p loss mediated KIF26B activation promoted hepatocellular carcinoma progression by activating PI3K/AKT pathway.

Hua Li, Shen Shen, Xiaolong Chen, Zhigang Ren, Zhiqin Li, Zujiang Yu

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Research progress of kinesin family in neurological diseases.Frontiers in cellular neuroscience · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Hua Li *1Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, 1# Jianshe East Road, Zhengzhou, 450052 China.
Shen Shen *1Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, 1# Jianshe East Road, Zhengzhou, 450052 China.
Xiaolong Chen1Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, 1# Jianshe East Road, Zhengzhou, 450052 China.
Zhigang Ren1Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, 1# Jianshe East Road, Zhengzhou, 450052 China.
Zhiqin Li1Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, 1# Jianshe East Road, Zhengzhou, 450052 China.
Zujiang Yu1Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, 1# Jianshe East Road, Zhengzhou, 450052 China.ORCID 0000-0003-0954-5472
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKinesin family member 26B (KIF26B) is unveiled acted as important role in many solid tumors, however, the function of KIF26B in hepatocellular carcinoma (HCC) is unclear.

methodsThe expression of KIF26B in HCC tissues and cell lines were measured with immunochemistry, real-time PCR and western blotting. The correlation between KIF26B expression and clinicopathological characteristics were analyzed by SPSS19.0. Functional experiments of KIF26B was conducted by CCK-8, transwell, EDU, colony formation in vitro and tumorigenesis in vivo. The gene set enrichment analysis was used to search the downstream pathway, luciferase reporter experiment was used to find the upstream regulatory factor of KIF26B.

resultsIn this study, we found that KIF26B was overexpressed both in HCC tissues and cell lines. High expression of KIF26B was associated with poor overall survival (OS), late TNM stage and poor differentiation. Loss of function experiments showed that suppression of KIF26B could inhibit cell viability, proliferation rate and invasion ability of HCC cells. KEGG and GO analysis showed that expression of KIF26B was highly relevant with PI3K/AKT signal pathway, and suppression of KIF26B could decrease the expression of m-TOR, p-PI3K and p-AKT. Further study demonstrated that expression of KIF26B was negative correlated with miR-450b-5p level in HCC tissues, and miR-450b-5p could inhibit cell viability, proliferation rate and invasion ability of HCC cells via targeted inhibiting KIF26B.

conclusionOur study demonstrated that miR-450-5p/KIF26B/AKT axis is critical for progression of HCC, and might provide novel prognostic biomarker and therapeutic target for HCC.

Indexed as

Hepatocellular carcinoma (HCC)Kinesin family member 26B (KIF26B)miR-450b-5pPI3K/AKT signal pathway

Identifiers

PMID31388332
PMCPMC6670205
OpenAlexW2964791713

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.