Evidence map›Paper›PMID 30569150›Full record

ArticleMolecular medicine reports2019

Autophagy flux inhibition mediated by celastrol sensitized lung cancer cells to TRAIL‑induced apoptosis via regulation of mitochondrial transmembrane potential and reactive oxygen species.

Uddin Md Nazim, Honghua Yin, Sang-Youel Park

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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  4. Autophagy in the pharmacological activities of celastrol (Review).Experimental and therapeutic medicine · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Uddin Md NazimDepartment of Biochemistry, Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk 54596, Republic of Korea.
Honghua YinDepartment of Biochemistry, Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk 54596, Republic of Korea.
Sang-Youel ParkDepartment of Biochemistry, Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk 54596, Republic of Korea.
Jeonbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor‑related apoptosis-inducing ligand (TRAIL) is well known as a transmembrane cytokine and has been proposed as one of the most effective anti‑cancer therapeutic agents, owing to its efficiency to selectively induce cell death in a variety of tumor cells. Suppression of autophagy flux has been increasingly acknowledged as an effective and novel therapeutic intervention for cancer. The present study demonstrated that the anti‑cancer and anti‑inflammatory drug celastrol, through its anti‑metastatic properties, may initiate TRAIL‑mediated apoptotic cell death in lung cancer cells. This sensitization was negatively affected by N‑acetyl‑l‑cysteine, which restored the mitochondrial membrane potential (ΔΨm) and inhibited reactive oxygen species (ROS) generation. Notably, treatment with celastrol caused an increase in microtubule‑associated proteins 1A/1B light chain 3B‑II and p62 levels, whereas co‑treatment of celastrol and TRAIL increased active caspase 3 and 8 levels compared with the control, confirming inhibited autophagy flux. The combined use of TRAIL with celastrol may serve as a safe and adequate therapeutic technique for the treatment of TRAIL‑resistant lung cancer, suggesting that celastrol‑mediated autophagy flux inhibition sensitized TRAIL‑initiated apoptosis via regulation of ROS and ΔΨm.

Indexed as

Gene Expression Regulation, NeoplasticA549 CellsAcetylcysteineAntineoplastic Agents, PhytogenicApoptosisAutophagyCaspase 8Cell Line, TumorChloroquineDrug CombinationsDrug SynergismHumansMembrane Potential, MitochondrialMicrotubule-Associated ProteinsMitochondriaPentacyclic TriterpenesAcetylcysteineAntineoplastic Agents, PhytogenicCASP8 protein, humanCaspase 8celastrolChloroquineDrug CombinationsMAP1LC3B protein, humanMicrotubule-Associated ProteinsPentacyclic TriterpenesReactive Oxygen SpeciesSequestosome-1 ProteinSQSTM1 protein, humanTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTriterpenesapoptosisautophagy fluxcancercelastroltumor necrosis factor‑related apoptosis-inducing ligand

Identifiers

PMID30569150
PMCPMC6323218
OpenAlexW2905275005

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.