Evidence map›Paper›PMID 26418898›Full record

ArticleOncotarget2016

Induction of methionine adenosyltransferase 2A in tamoxifen-resistant breast cancer cells.

Nguyen Thi Thuy Phuong, Sang Kyum Kim, Ji Hye Im, Jin Won Yang, Min Chang Choi, Sung Chul Lim, Kwang Yeol Lee, Young-Mi Kim, Jeong Hoon Yoon, Keon Wook Kang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

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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

10 authors at 6 institutions in 1 country.

Nguyen Thi Thuy PhuongCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, South Korea.
Sang Kyum KimCollege of Pharmacy, Chungnam National University, Daejeon 305-764, South Korea.
Ji Hye ImCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, South Korea.
Jin Won YangCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, South Korea.
Min Chang ChoiCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, South Korea.
Sung Chul LimDepartment of Pathology, College of Medicine, Chosun University, Gwangju 501-759, South Korea.
Kwang Yeol LeeCollege of Pharmacy, Chonnam National University, Gwangju 500-757, South Korea.
Young-Mi KimCollege of Pharmacy, Hanyang University, Ansan 426-791, South Korea.
Jeong Hoon YoonDepartment of Oral & Maxillofacial Pathology, College of Dentistry, Daejeon Dental Hospital, Wonkwang University, Daejeon 302-120, South Korea.
Keon Wook KangCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, South Korea.
Seoul National University · KRChonnam National University · KRChosun University · KRChungnam National University · KRHanyang University · KRWonkwang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously showed that S-adenosylmethionine-mediated hypermethylation of the PTEN promoter was important for the growth of tamoxifen-resistant MCF-7 (TAMR-MCF-7) cancer cells. Here, we found that the basal expression level of methionine adenosyltransferase 2A (MAT2A), a critical enzyme for the biosynthesis of S-adenosylmethionine, was up-regulated in TAMR-MCF-7 cells compared with control MCF-7 cells. Moreover, the basal expression level of MAT2A in T47D cells, a TAM-resistant estrogen receptor-positive cell line was higher compared to MCF-7 cells. Immunohistochemistry confirmed that MAT2A expression in TAM-resistant human breast cancer tissues was higher than that in TAM-responsive cases. The promoter region of human MAT2A contains binding sites for nuclear factor-κB, activator protein-1 (AP-1), and NF-E2-related factor 2 (Nrf2), and the activities of these three transcription factors were enhanced in TAMR-MCF-7 cells. Both the protein expression and transcriptional activity of MAT2A in TAMR-MCF-7 cells were potently suppressed by NF-κB inhibition but not by c-Jun/AP-1 or Nrf2 knock-down. Interestingly, the expression levels of microRNA (miR)-146a and -146b were diminished in TAMR-MCF-7 cells, and miR-146b transduction decreased NF-κB-mediated MAT2A expression. miR-146b restored PTEN expression via the suppression of PTEN promoter methylation in TAMR-MCF-7 cells. Additionally, miR-146b overexpression inhibited cell proliferation and reversed chemoresistance to 4-hydroxytamoxifen in TAMR-MCF-7 cells.

Indexed as

Drug Resistance, NeoplasmAntineoplastic Agents, HormonalApoptosisBiomarkers, TumorBreast NeoplasmsCell ProliferationDNA MethylationFemaleGene Expression Regulation, NeoplasticHumansMethionine AdenosyltransferaseMicroRNAsNF-E2-Related Factor 2NF-kappa BPromoter Regions, GeneticPTEN PhosphohydrolaseAntineoplastic Agents, HormonalBiomarkers, TumorMAT2A protein, humanMethionine AdenosyltransferaseMicroRNAsMIRN146 microRNA, humanNF-E2-Related Factor 2NF-kappa BPTEN PhosphohydrolasePTEN protein, humanS-AdenosylmethionineTamoxifenTranscription Factor AP-1MAT2AmiR-146bNF-κBPTENtamoxifen resistance

Identifiers

PMID26418898
PMCPMC4924687
OpenAlexW2172934950

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.