Evidence map›Paper›PMID 29138806›Full record

ArticleInternational journal of oncology2018

Effect of bis(hydroxymethyl) alkanoate curcuminoid derivative MTH-3 on cell cycle arrest, apoptotic and autophagic pathway in triple-negative breast adenocarcinoma MDA-MB-231 cells: An in vitro study.

Ling-Chu Chang, Min-Tsang Hsieh, Jai-Sing Yang, Chi-Cheng Lu, Fuu-Jen Tsai, Je-Wei Tsao, Yu-Jen Chiu, Sheng-Chu Kuo, Kuo-Hsiung Lee

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

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  12. 6-Methoxylated Flavonoids: Jacein, and 3-demethyljacein fromIranian journal of pharmaceutical research : IJPR · 2021
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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

9 authors at 3 institutions in 1 country.

Ling-Chu ChangChinese Medicinal Research and Development Center, China Medical University Hospital, Taichung 404, R.O.C.
Min-Tsang HsiehChinese Medicinal Research and Development Center, China Medical University Hospital, Taichung 404, R.O.C.
Jai-Sing YangDepartment of Medical Research, China Medical University Hospital, China Medical University, Taichung 404, R.O.C.
Chi-Cheng LuDepartment of Pharmacy, Buddhist Tzu Chi General Hospital, Hualien 970, Taiwan, R.O.C.
Fuu-Jen TsaiHuman Genetic Center, China Medical University Hospital, Taichung 404, R.O.C.
Je-Wei TsaoSchool of Pharmacy, China Medical University, Taichung 404, R.O.C.
Yu-Jen ChiuDivision of Reconstructive and Plastic Surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei 112, Taiwan, R.O.C.
Sheng-Chu KuoChinese Medicinal Research and Development Center, China Medical University Hospital, Taichung 404, R.O.C.
Kuo-Hsiung LeeChinese Medicinal Research and Development Center, China Medical University Hospital, Taichung 404, R.O.C.
China Medical University · TWBuddhist Tzu Chi General Hospital · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Curcumin has been shown to exert potential antitumor activity in vitro and in vivo involved in multiple signaling pathways. However, the application of curcumin is still limited because of its poor hydrophilicity and low bio-availability. In the present study, we investigated the therapeutic effects of a novel and water soluble bis(hydroxymethyl) alkanoate curcuminoid derivative, MTH-3, on human breast adenocarcinoma MDA-MB-231 cells. This study investigated the effect of MTH-3 on cell viability, cell cycle and induction of autophagy and apoptosis in MDA-MB-231 cells. After 24-h treatment with MTH-3, a concentration-dependent decrease in MDA-MB-231 cell viability was observed, and the IC50 value was 5.37±1.22 µM. MTH-3 significantly triggered G2/M phase arrest and apoptosis in MDA-MB-231 cells. Within a 24-h treatment, MTH-3 decreased the CDK1 activity by decreasing CDK1 and cyclin B1 protein levels. MTH-3-induced apoptosis was further confirmed by morphological assessment and annexin V/PI staining assay. Induction of apoptosis caused by MTH-3 was accompanied by an apparent increase of DR3, DR5 and FADD and, as well as a marked decrease of Bcl-2 and Bcl-xL protein expression. MTH-3 also decreased the protein levels of Ero1, PDI, PERK and calnexin, as well as increased the expression of IRE1α, CHOP and Bip that consequently led to ER stress and MDA-MB-231 cell apoptosis. In addition, MTH-3-treated cells were involved in the autophagic process and cleavage of LC3B was observed. MTH-3 enhanced the protein levels of LC3B, Atg5, Atg7, Atg12, p62 and Beclin-1 in MDA-MB-231 cells. Finally, DNA microarray was carried out to investigate the level changes of gene expression modulated by MTH-3 in MDA-MB-231 cells. Taken together, our results suggest that MTH-3 might be a novel therapeutic agent for the treatment of triple-negative breast cancer in the near future.

Indexed as

ApoptosisAutophagyCell Cycle CheckpointsCell Line, TumorCurcuminFemaleGene ExpressionHumansOligonucleotide Array Sequence AnalysisTriple Negative Breast NeoplasmsCurcumin

Identifiers

PMID29138806
PMCPMC5743386
OpenAlexW2768164643

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.