Evidence map›Paper›PMID 26782688›Full record

ArticleIrish journal of medical science2017

In vitro study of human mutL homolog 1 hypermethylation in inducing drug resistance of esophageal carcinoma.

Y Cao, Y Chen, Y Huang, Z Liu, G Li

Abstract read
PubMed Publisher
In one paragraph

Article in Irish journal of medical science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. 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

5 authors at 3 institutions in 1 country.

Y CaoDepartment of Thoracic Surgery, Central Hospital of Zaozhuang Mining Group of Shandong Province, Zaozhuang, 277800, Shandong, People's Republic of China.
Y ChenDepartment of Thoracic Surgery, Central Hospital of Zaozhuang Mining Group of Shandong Province, Zaozhuang, 277800, Shandong, People's Republic of China.
Y HuangDepartment of Thoracic Surgery, Central Hospital of Zaozhuang Mining Group of Shandong Province, Zaozhuang, 277800, Shandong, People's Republic of China.
Z LiuSecond Department of Liver Failure, No. 302 Hospital of PLA, Beijing, 100000, People's Republic of China.
G LiDepartment of Oncology, Affiliated Hospital of Weifang Medical University, #465 Yu He Road, Weifang, 261000, Shandong, People's Republic of China. weifangatjinan1984@163.com.
Zaozhuang Municipal Hospital · CN302 Military Hospital of China · CNWeifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAberrant promoter methylation of tumor suppressor gene can inhibit corresponding protein expression and promote carcinogenesis. Many studies have demonstrated that human mutL homolog 1(hMLH1) promoter methylation is correlated with occurrence and progression of multiple types of tumors. However, its correlation with esophageal carcinoma drug resistance is still unknown.

aimsTo confirm methylation status of hMLH1 promoter in drug-resistance cell line of esophageal carcinoma, further confirm whether hMLH1 promoter methylation is responsible for drug resistance.

methodsTwo stable esophageal carcinoma drug-resistance cell lines were successfully established by Cisplatin (DDP) concentration increment method; methylation status of hMLH1 promoter, mRNA and protein expression of hMLH1 were detected by methylation-specific PCR (MSP), RT-PCR and western blot, respectively; Drug-resistance ability assay was used to detect drug-resistance ability.

resultsStronger methylation status of hMLH1 promoter, lower hMLH1 mRNA and protein expression were found in both drug-resistance cell lines; after removing methylated bands using 5-aza-2'-deoxycytidine(5-Aza-CdR) in drug-resistance cell lines, hMLH1 mRNA and protein expression were restored and drug-resistance abilities declined nearly by half.

conclusionhMLH1 promoter hypermethylation plays important roles in esophageal carcinoma drug-resistance and show us the prospect that combination of demethylation treatment with conventional chemotherapy drugs may bring better therapy effect.

Indexed as

AzacitidineCell Line, TumorCisplatinDecitabineDNA MethylationDrug Resistance, NeoplasmEsophageal NeoplasmsHumansMutL Protein Homolog 1Promoter Regions, GeneticRNA, MessengerAzacitidineCisplatinDecitabineMutL Protein Homolog 1RNA, MessengerDrug-resistance cell lineEsophageal carcinomaHuman mutL homolog 1(hMLH1)Promoter methylation

Identifiers

PMID26782688
OpenAlexW2340932506

What OpenQuestion holds

Textmetadata
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.