Evidence map›Paper›PMID 28600513›Full record

ArticleScientific reports2017

TRPC5-induced autophagy promotes drug resistance in breast carcinoma via CaMKKβ/AMPKα/mTOR pathway.

Peng Zhang, Xiaoyu Liu, Hongjuan Li, Zhen Chen, Xiaoqiang Yao, Jian Jin, Xin Ma

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

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  6. Cecropin anisaxin-2S hasFrontiers in immunology · 2025
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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 2 institutions in 1 country.

Peng ZhangWuxi School of Medicine, Jiangnan University, Wuxi, China.
Xiaoyu LiuSchool of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, China.
Hongjuan LiSchool of Pharmaceutical Sciences, Jiangnan University, Wuxi, China.
Zhen ChenSchool of Pharmaceutical Sciences, Jiangnan University, Wuxi, China.
Xiaoqiang YaoSchool of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, China.
Jian JinSchool of Pharmaceutical Sciences, Jiangnan University, Wuxi, China. jinjian31@126.com.
Xin MaWuxi School of Medicine, Jiangnan University, Wuxi, China. maxin@jiangnan.edu.cn.
Jiangnan University · CNChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adriamycin is a first-line chemotherapy agent against cancer, but the development of resistance has become a major problem. Although autophagy is considered to be an adaptive survival response in response to chemotherapy and may be associated with chemoresistance, its inducer and the underlying molecular mechanisms remain unclear. Here, we demonstrate that adriamycin up-regulates the both levels of TRPC5 and autophagy, and the increase in autophagy is mediated by TRPC5 in breast cancer cells. Blockade of TRPC5 or autophagy increased the sensitivity to chemotherapy in vitro and in vivo. Notably, we revealed a positive correlation between TRPC5 and the autophagy-associated protein LC3 in paired patients with or without anthracycline-taxane-based chemotherapy. Furthermore, pharmacological inhibition and gene-silencing showed that the cytoprotective autophagy mediated by TRPC5 during adriamycin treatment is dependent on the CaMKKβ/AMPKα/mTOR pathway. Moreover, adriamycin-resistant MCF-7/ADM cells maintained a high basal level of autophagy, and silencing of TRPC5 and inhibition of autophagy counteracted the resistance to adriamycin. Thus, our results revealed a novel role of TRPC5 as an inducer of autophagy, and this suggests a novel mechanism of drug resistance in chemotherapy for breast cancer.

Indexed as

Gene Expression Regulation, NeoplasticAdenineAMP-Activated Protein KinasesAnimalsAntineoplastic Combined Chemotherapy ProtocolsAutophagyBreast NeoplasmsCalciumCalcium-Calmodulin-Dependent Protein Kinase KinaseCell Line, TumorDoxorubicinDrug Resistance, NeoplasmFemaleHumansMCF-7 CellsMice3-methyladenineAdenineAMP-Activated Protein KinasesCalciumCalcium-Calmodulin-Dependent Protein Kinase KinaseDoxorubicinMAP1LC3A protein, humanMicrotubule-Associated ProteinsMTOR protein, humanPRKAA1 protein, humanRNA, Small InterferingTaxoidsTOR Serine-Threonine KinasesTRPC5 protein, humanTRPC Cation Channels

Identifiers

PMID28600513
PMCPMC5466655
OpenAlexW2623356205

What OpenQuestion holds

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LicenceCC BY
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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.