Evidence map›Paper›PMID 32236584›Full record

ArticleOncology reports2020

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells.

Minyan Wei, Jiajun Li, Jianhua Qiu, Yanyan Yan, Hui Wang, Zengbao Wu, Yun Liu, Xiaoyun Shen, Chaoyue Su, Qiaoru Guo and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  8. Molecules (Basel, Switzerland) · 2022
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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

13 authors at 3 institutions in 1 country.

Minyan Wei *Guangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Jiajun Li *Guangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Jianhua Qiu *Guangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Yanyan YanDepartment of Pharmacology, Institute of Respiratory and Occupational Diseases, Collaborative Innovation Center for Cancer, Medical College, Shanxi Datong University, Datong, Shanxi 037009, P.R. China.
Hui WangDepartment of Thoracic Surgery, Guangzhou Institute of Pediatrics/Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong 510623, P.R. China.
Zengbao WuKey Laboratory of Xinjiang Phytomedicine Resources of Ministry of Education, School of Pharmacy, Shihezi University, Shihezi, Xinjiang 832000, P.R. China.
Yun LiuGuangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Xiaoyun ShenGuangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Chaoyue SuGuangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Qiaoru GuoGuangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Yanrui PanGuangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Peiquan ZhangGuangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Jianye ZhangGuangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Guangzhou Medical University · CNShanxi Datong University · CNShihezi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Costunolide being a sesquiterpene lactone, is known to have anticancer properties. The present study investigated the anticancer effects of costunolide against the H1299 human non‑small‑cell lung cancer (NSCLC) cell line. Inhibition of cell viability by costunolide was assessed via a MTT assay. Furthermore, the apoptotic rate was detected using Annexin V/propidium iodide labeling. A colony forming cell assay was performed to investigate the antiproliferative effects of costunolide. Wound healing and Transwell assays were performed to determine the inhibitory effects of costunolide on migration and invasion, respectively. Western blot analysis was undertaken to determine protein expression, and reverse transcription‑quantitative PCR was performed to assess mRNA expression levels. The results demonstrated that costunolide inhibited the viability of H1299 cells, with a half maximal inhibitory concentration value of 23.93±1.67 µM and induced cellular apoptosis in a dose‑dependent manner. Furthermore, the colony formation, migrative and invasive abilities of the H1299 cells were inhibited in a dose‑ or time‑dependent manner. The protein expression levels of E‑cadherin increased and those of N‑cadherin decreased following treatment with costunolide, which suggested that costunolide inhibited epithelial‑to‑mesenchymal transition. The mRNA levels of B‑Raf, E‑cadherin, N‑cadherin, integrins α2 and β1, as well as matrix metalloproteinases 2 were also found to be regulated costunolide. These findings indicate the potential of costunolide in the treatment of NSCLC.

Indexed as

Antineoplastic Agents, PhytogenicCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationCell SurvivalEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansLactonesLung NeoplasmsSesquiterpenesSignal TransductionAntineoplastic Agents, PhytogeniccostunolideLactonesSesquiterpenesanticancercostunolideepithelial-to-mesenchymal transitioninvasionmigrationnon-small-cell lung cancer

Identifiers

PMID32236584
PMCPMC7160540
OpenAlexW3013063052

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.