Evidence map›Paper›PMID 34681736›Full record

ArticleInternational journal of molecular sciences2021

OSMI-1 Enhances TRAIL-Induced Apoptosis through ER Stress and NF-κB Signaling in Colon Cancer Cells.

Su-Jin Lee, Da-Eun Lee, Soo-Young Choi, Oh-Shin Kwon

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Molecular medicine reports · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Beyond Traditional Use: The Scientific Evidence for the Role ofPharmaceuticals (Basel, Switzerland) · 2025
    Review
  9. Article
  10. Article
  11. Insights into O-GlcNAcylation and programmed cell death in cancer.Frontiers in cell and developmental biology · 2025
    Review
  12. Article
  13. Article
  14. O-GlcNAcylation: Crosstalk between Hemostasis, Inflammation, and Cancer.International journal of molecular sciences · 2024
    Review
  15. Review
  16. Review
  17. Article
  18. Application of Luteolin in Neoplasms and Nonneoplastic Diseases.International journal of molecular sciences · 2023
    Review
  19. Review
  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

4 authors at 2 institutions in 1 country.

Su-Jin LeeBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.
Da-Eun LeeBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.
Soo-Young ChoiDepartment of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea.
Oh-Shin KwonBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Korea.
Kyungpook National University · KRHallym University · KR

Funding

Kyungpook National University kyungpook National University Development Project Research Fund,2018National Research Foundation of Korea 2020R1A2B5B01001882
6 · The paper itself

Abstract

Levels of O-GlcNAc transferase (OGT) and hyper-O-GlcNAcylation expression levels are associated with cancer pathogenesis. This study aimed to find conditions that maximize the therapeutic effect of cancer and minimize tissue damage by combining an OGT inhibitor (OSMI-1) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). We found that OSMI-1 treatment in HCT116 human colon cancer cells has a potent synergistic effect on TRAIL-induced apoptosis signaling. Interestingly, OSMI-1 significantly increased TRAIL-mediated apoptosis by increasing the expression of the cell surface receptor DR5. ROS-induced endoplasmic reticulum (ER) stress by OSMI-1 not only upregulated CHOP-DR5 signaling but also activated Jun-N-terminal kinase (JNK), resulting in a decrease in Bcl2 and the release of cytochrome c from mitochondria. TRAIL induced the activation of NF-κB and played a role in resistance as an antiapoptotic factor. During this process, O-GlcNAcylation of IκB kinase (IKK) and IκBα degradation occurred, followed by translocation of p65 into the nucleus. However, combination treatment with OSMI-1 counteracted the effect of TRAIL-mediated NF-κB signaling, resulting in a more synergistic effect on apoptosis. Therefore, the combined treatment of OSMI-1 and TRAIL synergistically increased TRAIL-induced apoptosis through caspase-8 activation. Conclusively, OSMI-1 potentially sensitizes TRAIL-induced cell death in HCT116 cells through the blockade of NF-κB signaling and activation of apoptosis through ER stress response.

Indexed as

AnimalsApoptosisCell Line, TumorColonic NeoplasmsEndoplasmic Reticulum StressEndoribonucleasesEnzyme InhibitorsHumansMiceMice, NudeN-AcetylglucosaminyltransferasesNF-kappa BProtein Serine-Threonine KinasesReactive Oxygen SpeciesReceptors, TNF-Related Apoptosis-Inducing LigandRNA InterferenceEndoribonucleasesEnzyme InhibitorsERN1 protein, humanN-AcetylglucosaminyltransferasesNF-kappa BO-GlcNAc transferaseProtein Serine-Threonine KinasesReactive Oxygen SpeciesReceptors, TNF-Related Apoptosis-Inducing LigandRNA, Small InterferingTNF-Related Apoptosis-Inducing LigandTranscription Factor CHOPapoptosisER stressNF-κBO-GlcNAc transferase inhibitorTRAIL

Identifiers

PMID34681736
PMCPMC8539180
OpenAlexW3205265824

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.