Evidence map›Paper›PMID 26473737›Full record

ArticlePloS one2015

Celastrol Induces Autophagy by Targeting AR/miR-101 in Prostate Cancer Cells.

Jianquan Guo, Xuemei Huang, Hui Wang, Huanjie Yang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 76 citations in OpenAlex.

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  9. Withaferin A and Celastrol Overwhelm Proteostasis.International journal of molecular sciences · 2023
    Review
  10. Autophagy in the pharmacological activities of celastrol (Review).Experimental and therapeutic medicine · 2023
    Review
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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

4 authors at 1 institution in 1 country.

Jianquan GuoSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150001, China.
Xuemei HuangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150001, China.
Hui WangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150001, China.
Huanjie YangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150001, China.
Harbin Institute of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an evolutionarily conserved process responsible for the degradation and recycling of cytoplasmic components through autolysosomes. Targeting AR axis is a standard strategy for prostate cancer treatment; however, the role of AR in autophagic processes is still not fully understood. In the present study, we found that AR played a negative role in AR degrader celastrol-induced autophagy. Knockdown of AR in AR-positive prostate cancer cells resulted in enhanced autophagy. Ectopic expression of AR in AR-negative prostate cancer cells, or gain of function of the AR signaling in AR-positive cells, led to suppression of autophagy. Since miR-101 is an inhibitor of autophagy and its expression was decreased along with AR in the process of celastrol-induced autophagy, we hypothesize that AR inhibits autophagy through transactivation of miR-101. AR binding site was defined in the upstream of miR-101 gene by luciferase reporter and ChIP assays. MiR-101 expression correlated with AR status in prostate cancer cell lines. The inhibition of celastrol-induced autophagy by AR was compromised by blocking miR-101; while transfection of miR-101 led to inhibition of celastrol-induced autophagy in spite of AR depletion. Furthermore, mutagenesis of the AR binding site in miR-101 gene led to decreased suppression of autophagy by AR. Finally, autophagy inhibition by miR-101 mimic was found to enhance the cytotoxic effect of celastrol in prostate cancer cells. Our results demonstrate that AR inhibits autophagy via transactivation of miR-101, thus combination of miR-101 mimics with celastrol may represent a promising therapeutic approach for treating prostate cancer.

Indexed as

Drug Delivery SystemsAutophagyCell Line, TumorGene Expression Regulation, NeoplasticHumansMaleMicroRNAsNeoplasm ProteinsPentacyclic TriterpenesProstatic NeoplasmsReceptors, AndrogenRNA, NeoplasmTriterpenesAR protein, humancelastrolMicroRNAsMIRN101 microRNA, humanNeoplasm ProteinsPentacyclic TriterpenesReceptors, AndrogenRNA, NeoplasmTriterpenes

Identifiers

PMID26473737
PMCPMC4608724
OpenAlexW2252856015

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.