Evidence map›Paper›PMID 31524219›Full record

ArticleInternational journal of molecular medicine2019

Alantolactone enhances gemcitabine sensitivity of lung cancer cells through the reactive oxygen species-mediated endoplasmic reticulum stress and Akt/GSK3β pathway.

Jiquan Wang, Yingbing Zhang, Xu Liu, Jizhao Wang, Bin Li, Yongkang Liu, Jiansheng Wang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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, 29 citations in OpenAlex.

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  8. Elecampane (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

7 authors at 2 institutions in 1 country.

Jiquan WangDepartment of Radiation Oncology, The First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Yingbing ZhangDepartment of Radiation Oncology, The First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Xu LiuDepartment of Thoracic Surgery, The First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Jizhao WangDepartment of Thoracic Surgery, The First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Bin LiKey Laboratory of Resource Biology and Biotechnology in Western China, Northwest University, Xi'an, Shaanxi 710069, P.R. China.
Yongkang LiuKey Laboratory of Resource Biology and Biotechnology in Western China, Northwest University, Xi'an, Shaanxi 710069, P.R. China.
Jiansheng WangDepartment of Thoracic Surgery, The First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
First Affiliated Hospital of Xi'an Jiaotong University · CNNorthwest University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is one of the leading causes of cancer‑associated mortality in China and globally. Gemcitabine (GEM), as a first‑line therapeutic drug, has been used to treat lung cancer, but GEM resistance poses a major limitation on the efficacy of GEM chemotherapy. Alantolactone (ALT), a sesquiterpene lactone compound isolated from Inula helenium, has been identified to exert anticancer activity in various types of cancer, including breast, pancreatic, lung squamous and colorectal cancer. However, the underlying mechanisms of the anticancer activity of ALT in lung cancer remain to be fully elucidated. The present study aimed to determine whether ALT enhances the anticancer efficacy of GEM in lung cancer cells and investigated the underlying mechanisms. The cell viability was assessed with a Cell Counting Kit‑8 assay. The cell cycle, apoptosis and the level of reactive oxygen species (ROS) were assessed by flow cytometry, and the expression of cell cycle‑associated and apoptosis‑associated proteins were determined by western blot analysis. The results demonstrated that ALT inhibited cell growth and induced S‑phase arrest and cell apoptosis in A549 and NCI‑H520 cells. Furthermore, ALT increased the level of ROS, inhibited the Akt/glycogen synthase kinase (GSK)3β pathway and induced endoplasmic reticulum (ER) stress in A549 and NCI‑H520 cells. Additionally, ALT treatment sensitized lung cancer cells to GEM. Analysis of the molecular mechanisms further revealed that ALT enhanced the anticancer effects of GEM via ROS‑mediated activation of the Akt/GSK3β and ER stress pathways. In conclusion, combined treatment with ALT and GEM may have potential as a clinical strategy for lung cancer treatment.

Indexed as

ApoptosisCell CycleCell Line, TumorCell ProliferationDeoxycytidineDrug Resistance, NeoplasmEndoplasmic Reticulum StressGemcitabineGlycogen Synthase Kinase 3 betaHumansLactonesLung NeoplasmsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSesquiterpenes, EudesmaneSignal TransductionalantolactoneDeoxycytidineGemcitabineGlycogen Synthase Kinase 3 betaLactonesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSesquiterpenes, Eudesmane

Identifiers

PMID31524219
PMCPMC6657978
OpenAlexW2959200286

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.