Evidence map›Paper›PMID 33302959›Full record

ArticleWorld journal of surgical oncology2020

ALKBH2 inhibition alleviates malignancy in colorectal cancer by regulating BMI1-mediated activation of NF-κB pathway.

Bingxin Ke, Kejun Ye, Shaobing Cheng

Open access · goldAbstract read
In one paragraph

Article in World journal of surgical oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Predictive Analysis and Validation of Critical Missense SNPs of theInternational journal of molecular sciences · 2025
    Review
  4. Structural Analysis of the AlkB Family in Poultry.Animals : an open access journal from MDPI · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. 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

3 authors at 2 institutions in 1 country.

Bingxin KeDepartment of Colorectal Surgery, the First Affiliated Hospital, College of Medicine, Zhejiang University, No. 79, Qingchun Road, Xiacheng District, Hangzhou City, 310003, Zhejiang Province, China. 1514012@zju.edu.cn.ORCID http://orcid.org/0000-0003-4279-3195
Kejun YeDepartment of Colorectal Surgery, the First Affiliated Hospital, College of Medicine, Zhejiang University, No. 79, Qingchun Road, Xiacheng District, Hangzhou City, 310003, Zhejiang Province, China.
Shaobing ChengDepartment of Colorectal Surgery, the First Affiliated Hospital, College of Medicine, Zhejiang University, No. 79, Qingchun Road, Xiacheng District, Hangzhou City, 310003, Zhejiang Province, China.
Zhejiang University · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe alkB homolog 2, alpha-ketoglutarate-dependent dioxygenase (ALKBH2) gene is involved in DNA repair and is expressed in different types of malignancies. However, the role of ALKBH2 in colorectal carcinoma (CRC) remains unclear. This study aimed to explore the potential mechanism of ALKBH2 and its function in CRC.

methodsThe expression levels of ALKBH2 in CRC tissues and cells were determined by qRT-PCR. Following that, the role of ALKBH2 in cell proliferation, invasion, and epithelial-mesenchymal transition (EMT) in CRC cells (Caco-2 and LOVO) were assessed by Cell Counting Kit-8 (CCK-8), transwell assays, and Western blotting, respectively. The effect of ALKBH2 on B cell-specific Moloney murine leukemia virus integration site 1 (BMI1) and downstream NF-κB pathway was determined by Western blotting and luciferase reporter assay.

resultsThe expression of ALKBH2 was significantly upregulated both in CRC tissues and cells. Further experiments demonstrated that reduction of ALKBH2 suppressed Caco-2 and LOVO cell proliferation and invasion. Moreover, ALKBH2 knockdown also suppressed EMT, which increased E-cadherin expression and reduced N-cadherin expression. Besides, ALKBH2 silencing inhibited BMI1 expression and reduced nuclear accumulation of the NF-κB p65 protein, as well as the luciferase activity of NF-κB p65. Upregulation of BMI1 reversed the effect of ALKBH2 knockdown on the proliferation and invasion in CRC cells.

conclusionsOur findings suggest that suppression of ALKBH2 alleviates malignancy in CRC by regulating BMI1-mediated activation of NF-κB pathway. ALKBH2 may serve as a potential treatment target for human CRC.

Indexed as

Colorectal NeoplasmsNF-kappa BAlkB Homolog 2, Alpha-Ketoglutarate-Dependent DioxygenaseCaco-2 CellsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansPolycomb Repressive Complex 1PrognosisProto-Oncogene ProteinsALKBH2 protein, humanAlkB Homolog 2, Alpha-Ketoglutarate-Dependent DioxygenaseBMI1 protein, humanBmi1 protein, mouseNF-kappa BPolycomb Repressive Complex 1Proto-Oncogene ProteinsalkB homolog 2Alpha-ketoglutarate dependent dioxygenaseB cell-specific Moloney murine leukemia virus integration site 1Colorectal carcinomaNF-κB pathway

Identifiers

PMID33302959
PMCPMC7731553
OpenAlexW3111353626

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.