Evidence map›Paper›PMID 27689333›Full record

ArticleOncotarget2016

Curcumin targets the TFEB-lysosome pathway for induction of autophagy.

Jianbin Zhang, Jigang Wang, Jian Xu, Yuanqiang Lu, Jiukun Jiang, Liming Wang, Han-Ming Shen, Dajing Xia

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
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 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

69 citing papers in PubMed, 129 citations in OpenAlex.

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9 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 2 countries.

Jianbin ZhangClinical Research Institute, Zhejiang Provincial People's Hospital, Hangzhou, China.
Jigang WangDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Jian XuSchool of Public Health, Zhejiang University, Institute of Immunology, Zhejiang University, Hangzhou, China.
Yuanqiang LuFirst Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Jiukun JiangFirst Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Liming WangDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Han-Ming ShenDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Dajing XiaSchool of Public Health, Zhejiang University, Institute of Immunology, Zhejiang University, Hangzhou, China.
National University of Singapore · SGZhejiang University · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Curcumin is a hydrophobic polyphenol derived from the herb Curcumalonga and its wide spectrum of pharmacological activities has been widely studied. It has been reported that Curcumin can induce autophagy through inhibition of the Akt-mTOR pathway. However, the effect of Curcumin on lysosome remains largely elusive. In this study, we first found that Curcumin treatment enhances autophagic flux in both human colon cancer HCT116 cells and mouse embryonic fibroblasts (MEFs). Moreover, Curcumin treatment promotes lysosomal function, evidenced by the increased lysosomal acidification and enzyme activity. Second, Curcumin is capable of suppressing the mammalian target of rapamycin (mTOR). Interestingly, Curcumin fails to inhibit mTOR and to activate lysosomal function in Tsc2-/-MEFs with constitutive activation of mTOR, indicating that Curcumin-mediated lysosomal activation is achieved via suppression of mTOR. Third, Curcumin treatment activates transcription factor EB (TFEB), a key nuclear transcription factor in control of autophagy and lysosome biogenesis and function, based on the following observations: (i) Curcumin directly binds to TFEB, (ii) Curcumin promotes TFEB nuclear translocation; and (iii) Curcumin increases transcriptional activity of TFEB. Finally, inhibition of autophagy and lysosome leads to more cell death in Curcumin-treated HCT116 cells, suggesting that autophagy and lysosomal activation serves as a cell survival mechanism to protect against Curcumin-mediated cell death. Taken together, data from our study provide a novel insight into the regulatory mechanisms of Curcumin on autophagy and lysosome, which may facilitate the development of Curcumin as a potential cancer therapeutic agent.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicAutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell LineCell SurvivalCurcuminFibroblastsGene Knockout TechniquesHCT116 CellsHumansLysosomesMiceProtein BindingSignal TransductionTOR Serine-Threonine KinasesAntineoplastic Agents, PhytogenicBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCurcuminMTOR protein, humanTFEB protein, humanTOR Serine-Threonine KinasesautophagyCurcuminlysosomemTORTFEB

Identifiers

PMID27689333
PMCPMC5342768
OpenAlexW2525996450

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.