Evidence map›Paper›PMID 31052354›Full record

ArticleMolecules (Basel, Switzerland)2019

Heme Oxygenase-1 is a Key Molecule Underlying Differential Response of TW-37-Induced Apoptosis in Human Mucoepidermoid Carcinoma Cells.

In-Hyoung Yang, Chi-Hyun Ahn, Nam-Pyo Cho, Bohwan Jin, WonWoo Lee, Yun Chan Jung, Seong Doo Hong, Ji-Ae Shin, Sung-Dae Cho

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Hemoxygenase-1 Promotes Head and Neck Cancer Cell Viability.Antioxidants (Basel, Switzerland) · 2022
    Article
  3. Article
  4. 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

9 authors at 3 institutions in 1 country.

In-Hyoung YangDepartment of Oral Pathology, School of Dentistry, Institute of Oral Bioscience, Chonbuk National University, Jeonju 54896, Korea. inhyoung3@naver.com.
Chi-Hyun AhnDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 03080, Korea. chihyun610@snu.ac.kr.
Nam-Pyo ChoDepartment of Oral Pathology, School of Dentistry, Institute of Oral Bioscience, Chonbuk National University, Jeonju 54896, Korea. npcho@jbnu.ac.kr.
Bohwan JinLaboratory Animal Center, CHA University, CHA Biocomplex, Sampyeong-dong, Seongnam 13488, Korea. jnbhwan@cha.ac.kr.
WonWoo LeeLaboratory Animal Center, CHA University, CHA Biocomplex, Sampyeong-dong, Seongnam 13488, Korea. lsw232@chamc.co.kr.
Yun Chan JungChaon, Seongnamsi 13488, Korea. chaon@chaon.kr.
Seong Doo HongDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 03080, Korea. hongsd@snu.ac.kr.
Ji-Ae ShinDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 03080, Korea. sky21sm@snu.ac.kr.
Sung-Dae ChoDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 03080, Korea. efiwdsc@snu.ac.kr.ORCID 0000-0001-8670-9579
Seoul National University · KRCHA University · KRJeonbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TW-37 is a small-molecule inhibitor of Bcl-2 family proteins, which can induce anti-cancer activities in various types of cancer. In the current study, we investigated the potential molecular mechanism underlying the differential response to TW-37-induced apoptosis in two human mucoepidermoid carcinoma (MEC) cell lines. The differential response and underlying molecular mechanism of human MEC cells to TW-37 was evaluated by trypan blue exclusion assay, western blotting, 4', 6-diamidino-2-phenylindole staining, annexin V/propidium iodide double staining, analysis of the sub-G1 population, human apoptosis array, and measurements of intracellular reactive oxygen species (ROS). TW-37 decreased cell viability and induced apoptosis in YD-15 cells, but not in MC3 cells. Proteome profiling using a human apoptosis array revealed four candidate proteins and of these, heme oxygenase-1 (HO-1) was mainly related to the differential response to TW-37 of YD-15 and MC3 cells. TW-37 also led to a significant increase in intracellular levels of ROS in YD-15 cells, which is associated with apoptosis induction. The ectopic expression of HO-1 recovered YD-15 cells from TW-37-induced apoptosis by reducing intracellular levels of ROS. The expression of HO-1 was reduced through both transcriptional and post-translational modification during TW-37-mediated apoptosis. We conclude that HO-1 is a potential indicator to estimate response to TW37-induced apoptosis in human MEC.

Indexed as

BenzamidesCarcinoma, MucoepidermoidCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHeme Oxygenase-1HumansProtein Processing, Post-TranslationalProteomicsReactive Oxygen SpeciesSulfonesBenzamidesHeme Oxygenase-1HMOX1 protein, humanReactive Oxygen SpeciesSulfonesTW-37 compoundapoptosisheme oxygenase-1mucoepidermoid carcinomareactive oxygen speciesTW-37

Identifiers

PMID31052354
PMCPMC6539960
OpenAlexW2943109078

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.