Evidence map›Paper›PMID 27526942›Full record

ArticleJournal of biomedical science2016

CSC-3436 switched tamoxifen-induced autophagy to apoptosis through the inhibition of AMPK/mTOR pathway.

Sheng-Tang Wu, Guang-Huan Sun, Tai-Lung Cha, Chien-Chang Kao, Sun-Yran Chang, Sheng-Chu Kuo, Tzong-Der Way

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 45 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

7 authors at 3 institutions in 1 country.

Sheng-Tang WuDivision of Urology, Department of Surgery, Tri-Service General Hospital and National Defense Medical Center, Taichung, Taiwan.
Guang-Huan SunDivision of Urology, Department of Surgery, Tri-Service General Hospital and National Defense Medical Center, Taichung, Taiwan.
Tai-Lung ChaDivision of Urology, Department of Surgery, Tri-Service General Hospital and National Defense Medical Center, Taichung, Taiwan.
Chien-Chang KaoDivision of Urology, Department of Surgery, Tri-Service General Hospital and National Defense Medical Center, Taichung, Taiwan.
Sun-Yran ChangDivision of Urology, Department of Surgery, Tri-Service General Hospital and National Defense Medical Center, Taichung, Taiwan.
Sheng-Chu KuoSchool of Pharmacy, College of Pharmacy, China Medical University, Taichung, Taiwan. professor.kuo@gmail.com.
Tzong-Der WayDepartment of Biological Science and Technology, College of Biopharmaceutical and Food Sciences, China Medical University, No. 91 Hsueh-Shih Road, Taichung, 40402, Taiwan R.O.C. tdway@mail.cmu.edu.tw.
National Defense Medical Center · TWChina Medical University · TWTri-Service General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTriple-negative breast cancer (TNBC) lacks specific therapeutic target and limits to chemotherapy and is essential to develop novel therapeutic regimens. Increasing studies indicated that tamoxifen, a selective estrogen receptor modulators (SERMs), has anti-tumor therapeutic effect in estrogen receptor α (ERα)-negative tumor. Here, we determined whether autophagy was activated by tamoxifen in TNBC cells. Moreover, CSC-3436 displayed strong and selective growth inhibition on cancer cells. Next, we investigated the anti-proliferation effect of combination of CSC-3436 plus tamoxifen on cell death in TNBC cells.

resultsOur study found that tamoxifen induces autophagy in TNBC cells. Endoplasmic reticulum stress and AMPK/mTOR contributed tamoxifen-induced autophagy. Interestingly, in combination treatment with CSC-3436 enhanced the anti-proliferative effect of tamoxifen. We found that CSC-3436 switched tamoxifen-induced autophagy to apoptosis via cleavage of ATG-5. Moreover, AMPK/mTOR pathway may involve in CSC-3436 switched tamoxifen-induced autophagy to apoptosis. The combination of tamoxifen and CSC-3436 produced stronger tumor growth inhibition compared with CSC-3436 or tamoxifen alone treatments in vivo.

conclusionThese data indicated that CSC-3436 combined with tamoxifen may be a potential approach for treatment TNBC.

Indexed as

AMP-Activated Protein KinasesApoptosisAutophagyBreast NeoplasmsCell Line, TumorFemaleHumansNeoplasm ProteinsSignal TransductionTamoxifenTOR Serine-Threonine KinasesAMP-Activated Protein KinasesMTOR protein, humanNeoplasm ProteinsTamoxifenTOR Serine-Threonine KinasesAMPK/mTORCSC-3436Endoplasmic reticulum stressTamoxifenTriple-negative breast cancer

Identifiers

PMID27526942
PMCPMC4986227
OpenAlexW2516277153

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.