Evidence map›Paper›PMID 26633711›Full record

ArticleCell death & disease2015

Akt inhibition attenuates rasfonin-induced autophagy and apoptosis through the glycolytic pathway in renal cancer cells.

Q Lu, S Yan, H Sun, W Wang, Y Li, X Yang, X Jiang, Y Che, Z Xi

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 63 citations in OpenAlex.

  1. Myeloid-derived suppressor cells modulation in the context of tumor microenvironment for gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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  18. Regulation of Autophagy by Glycolysis in Cancer.Cancer management and research · 2020
    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

9 authors at 4 institutions in 1 country.

Q LuState Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
S YanState Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
H SunState Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
W WangState Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Y LiState Key Laboratory of Toxicology and Medical Countermeasures, Beijing Institute of Pharmacology and Toxicology, AMMS, Beijing, China.
X YangDepartment of Urology, Peking University First Hospital, Beijing, China.
X JiangState Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Y CheState Key Laboratory of Toxicology and Medical Countermeasures, Beijing Institute of Pharmacology and Toxicology, AMMS, Beijing, China.
Z XiDepartment of Urology, Peking University First Hospital, Beijing, China.
Chinese Academy of Sciences · CNInstitute of Microbiology · CNPeking University · CNPeking University First Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rasfonin is a fungal secondary metabolite with demonstrated antitumor effects. However, the underlying mechanism of the regulatory role in autophagy initiated by rasfonin is largely unknown. Moreover, the function of Akt to positively mediate the induced autophagy remains elusive. In the present study, we observed that rasfonin induced autophagy concomitant with the upregulation of Akt phosphorylation. Both the inhibition of Akt by small molecule inhibitors and genetic modification partially reduced rasfonin-dependent autophagic flux and PARP-1 cleavage. The overexpression of myrAkts (constant active form) promoted rasfonin-induced apoptosis and autophagy in a cell type- and Akt isoform-specific manner. Using quantitative PCR and immunoblotting, we observed that rasfonin increased the expression of glycolytic gene PFKFB3, and this increased expression can be suppressed in the presence of Akt inhibitor. The inhibition of PFKFB3 suppressed rasfonin-activated autophagy with enhanced PARP-1 cleavage. In the case of glucose uptake was disrupted, which mean the glycolytic pathway was fully blocked, the rasfonin-induced autophagy and PARP-1 cleavage were downregulated. Collectively, these results demonstrated that Akt positively regulated rasfonin-enhanced autophagy and caspase-dependent apoptosis primarily through affecting the glycolytic pathway.

Indexed as

ApoptosisAutophagyCarcinoma, Renal CellCell Line, TumorDrug InteractionsFatty Acids, UnsaturatedGlycolysisHeLa CellsHumansKidney NeoplasmsPhosphofructokinase-2PhosphorylationProtein Kinase InhibitorsProto-Oncogene Proteins c-aktPyronesTransfectionFatty Acids, UnsaturatedPFKFB3 protein, humanPhosphofructokinase-2Protein Kinase InhibitorsProto-Oncogene Proteins c-aktPyronesrasfonin

Identifiers

PMID26633711
PMCPMC4720880
OpenAlexW2186706269

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.