Evidence map›Paper›PMID 33019464›Full record

ArticleMedicine2020

The molecular mechanisms of celecoxib in tumor development.

Bin Wen, Ying-Ting Wei, Lan-Lan Mu, Guo-Rong Wen, Kui Zhao

Open access · goldAbstract read
In one paragraph

Article in Medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  11. Celecoxib in oncology: targeting the COX-2/PGEFrontiers in pharmacology · 2025
    Review
  12. Celecoxib inhibits NLRP1 inflammasome pathway in MDA-MB-231 Cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Article
  13. Review
  14. Article
  15. Article
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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 4 countries.

Bin WenDepartment of Gastroenterology, Affiliated Hospital to Zunyi Medical University, Zunyi, Guizhou Province, China.ORCID 0000-0001-8413-0037
Ying-Ting Wei
Lan-Lan Mu
Guo-Rong Wen
Kui Zhao
Zunyi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClinical studies have shown that celecoxib can significantly inhibit the development of tumors, and basic experiments and in vitro experiments also provide a certain basis, but it is not clear how celecoxib inhibits tumor development in detail.

methodsA literature search of all major academic databases was conducted (PubMed, China National Knowledge Internet (CNKI), Wan-fang, China Science and Technology Journal Database (VIP), including the main research on the mechanisms of celecoxib on tumors.

resultsCelecoxib can intervene in tumor development and reduce the formation of drug resistance through multiple molecular mechanisms.

conclusionCelecoxib mainly regulates the proliferation, migration, and invasion of tumor cells by inhibiting the cyclooxygenases-2/prostaglandin E2 signal axis and thereby inhibiting the phosphorylation of nuclear factor-κ-gene binding, Akt, signal transducer and activator of transcription and the expression of matrix metalloproteinase 2 and matrix metalloproteinase 9. Meanwhile, it was found that celecoxib could promote the apoptosis of tumor cells by enhancing mitochondrial oxidation, activating mitochondrial apoptosis process, promoting endoplasmic reticulum stress process, and autophagy. Celecoxib can also reduce the occurrence of drug resistance by increasing the sensitivity of cancer cells to chemotherapy drugs.

Indexed as

ApoptosisAutophagyCelecoxibCell ProliferationCyclooxygenase 2 InhibitorsDinoprostoneDrug Resistance, NeoplasmEndoplasmic Reticulum StressHumansMatrix Metalloproteinase 2Matrix Metalloproteinase 9MitochondriaNeoplasmsPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionCelecoxibCyclooxygenase 2 InhibitorsDinoprostoneMatrix Metalloproteinase 2Matrix Metalloproteinase 9Proto-Oncogene Proteins c-akt

Identifiers

PMID33019464
PMCPMC7535670
OpenAlexW3090745705

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.