Evidence map›Paper›PMID 36371217›Full record

ArticleJournal of translational medicine2022

Celastrol elicits antitumor effects by inhibiting the STAT3 pathway through ROS accumulation in non-small cell lung cancer.

Zhucheng Zhao, Yanmao Wang, Yuyan Gong, Xian Wang, Luyao Zhang, Haiyang Zhao, Jifa Li, Jiandong Zhu, Xiaoying Huang, Chengguang Zhao and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
12.0field-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

24 citing papers in PubMed, 41 citations in OpenAlex.

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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

12 authors at 4 institutions in 1 country.

Zhucheng Zhao *The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Yanmao Wang *The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Yuyan Gong *The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Xian WangThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Luyao ZhangThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Haiyang ZhaoThe Institute of Life Sciences, Wenzhou University, Wenzhou, 325035, Zhejiang, China.
Jifa LiAffiliated Yueqing Hospital, Wenzhou Medical University, Wenzhou, 325600, Zhejiang, China.
Jiandong ZhuAffiliated Yueqing Hospital, Wenzhou Medical University, Wenzhou, 325600, Zhejiang, China.
Xiaoying HuangThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.
Chengguang ZhaoThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. zhaochengguang@wmu.edu.cn.
Lehe YangThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. yanglehe@wmu.edu.cn.
Liangxing WangThe First Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. wzyxywlx@163.com.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CNFirst People's Hospital of Jingzhou · CNWenzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) is the most common lung cancer with high mortality across the world, but it is challenging to develop an effective therapy for NSCLC. Celastrol is a natural bioactive compound, which has been found to possess potential antitumor activity. However, the underlying molecular mechanisms of celastrol activity in NSCLC remain elusive.

methodsCellular function assays were performed to study the suppressive role of celastrol in human NSCLC cells (H460, PC-9, and H520) and human bronchial epithelial cells BEAS-2B. Cell apoptosis levels were analyzed by flow cytometry, Hoechst 33342, caspase-3 activity analysis, and western blot analysis. Intracellular reactive oxygen species (ROS) were analyzed by flow cytometry and fluorescence microscope. Expression levels of endoplasmic reticulum (ER) stress-related proteins and phosphorylated signal transducer and activator of transcription 3 (P-STAT3) were identified via western blot analysis. A heterograft model in nude mice was employed to evaluate the effect of celastrol in vivo.

resultsCelastrol suppressed the growth, proliferation, and metastasis of NSCLC cells. Celastrol significantly increased the level of intracellular ROS; thus, triggering the activation of the ER stress pathway and inhibition of the P-STAT3 pathway, and eventually leading to cell apoptosis, and the effects were reversed by the pre-treatment with N-Acetyl-L-cysteine (NAC). Celastrol also suppressed tumor growth in vivo.

conclusionThe outcomes revealed that celastrol plays a potent suppressive role in NSCLC in vitro and in vivo. Celastrol induces apoptosis via causing mitochondrial ROS accumulation to suppress the STAT3 pathway. Celastrol may have potential application prospects in the therapy of NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAnimalsApoptosisCell Line, TumorCell ProliferationHumansMiceMice, NudePentacyclic TriterpenesReactive Oxygen SpeciesSTAT3 Transcription FactorcelastrolPentacyclic TriterpenesReactive Oxygen SpeciesSTAT3 protein, humanSTAT3 Transcription FactorCelastrolInhibitorNSCLCROSSTAT3

Identifiers

PMID36371217
PMCPMC9652895
OpenAlexW4309072616

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.