Evidence map›Paper›PMID 31905343›Full record

ArticleAging2020

Aspirin enhances the sensitivity of colon cancer cells to cisplatin by abrogating the binding of NF-κB to the COX-2 promoter.

Wei Jiang, Yue Yan, Manyu Chen, Guangyu Luo, Jiaojiao Hao, Jinjin Pan, Sheng Hu, Ping Guo, Wenyang Li, Ruozu Wang and 10 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. 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
5.4field-weighted citation impact, top 4% 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, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Aspirin-induced acetylation of APE1/Ref-1 enhances RAGE binding and promotes apoptosis in ovarian cancer cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  8. Review
  9. HBXIP induces PARP1 via WTAP-mediated mActa pharmacologica Sinica · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Blockade of store-operated calcium entry sensitizes breast cancer cells to cisplatin therapy via modulating inflammatory response.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Pro-Inflammatory Signalling PRRopels Cisplatin-Induced Toxicity.International journal of molecular sciences · 2022
    Review
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

20 authors at 5 institutions in 1 country.

Wei JiangInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Yue YanSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Manyu ChenInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Guangyu LuoSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Jiaojiao HaoInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Jinjin PanInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Sheng HuInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Ping GuoInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Wenyang LiInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Ruozu WangInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Yan ZuoInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Yao SunInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Silei SuiInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Wendan YuInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Zhe PanInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Kun ZouInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Zongheng ZhengThe Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Wuguo DengSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Xiaojun WuSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Wei GuoInstitute of Cancer Stem Cells and The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Dalian Medical University · CNFirst Affiliated Hospital of Dalian Medical University · CNSun Yat-sen University Cancer Center · CNState Key Laboratory of Oncology in South ChinaThird Affiliated Hospital of Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin is one of the most potent chemotherapeutic agents for the treatment of colon cancer. Nevertheless, the unavoidability of the notable toxicity and the development of the acquired resistance severely restricted its clinical application. Aspirin and some other non-steroidal anti-inflammatory drugs have been used to prevent colon tumorigenesis as chemopreventive agents. Here, we explored the possibility of aspirin as an adjuvant drug to boost the anti-cancer effect of cisplatin for colon cancer. We found that aspirin significantly enhanced the cisplatin-mediated inhibitions of cell proliferation, migration and invasion and the induction of apoptosis in colon cancer cells. The combined treatment of aspirin and cisplatin suppressed the expression of the anti-apoptotic protein Bcl-2 and the EMT-related proteins, up-regulated the levels of the cleaved PARP and Bax, and blocked the PI3K/AKT and RAF-MEK-ERK signaling pathway. In addition, we demonstrated that the enhanced effect of aspirin on the cisplatin-induced inhibition of tumor cell growth was also mediated through the suppression of the binding activity of NF-κB to the COX-2 promoter. The combination of aspirin and cisplatin effectively attenuated the translocation of NF-κB p65/p50 from the cytoplasm to the nucleus, and abrogated the binding of NF-κB p65/p50 to the COX-2 promoter, thereby down-regulating COX-2 expression and PGE

Indexed as

AnimalsAntineoplastic AgentsApoptosisAspirinCell Line, TumorCell ProliferationCisplatinCyclooxygenase 2Drug SynergismHeterograftsHumansMiceNF-kappa BProtein BindingSignal TransductionAntineoplastic AgentsAspirinCisplatinCyclooxygenase 2NF-kappa Baspirincisplatincolon cancerCOX-2NF-κB

Identifiers

PMID31905343
PMCPMC6977689
OpenAlexW2999346926

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.