Evidence map›Paper›PMID 31496655›Full record

ArticleDrug design, development and therapy2019

Thapsigargin induces apoptosis in adrenocortical carcinoma by activating endoplasmic reticulum stress and the JNK signaling pathway: an in vitro and in vivo study.

Lili Wu, Xuemei Huang, Yaqi Kuang, Zengmiao Xing, Xiujun Deng, Zuojie Luo

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

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  19. Store-Operated CaInternational journal of molecular sciences · 2022
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  20. Role of Glycated High Mobility Group Box-1 in Gastric Cancer.International journal of molecular sciences · 2021
    Article
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

6 authors at 2 institutions in 1 country.

Lili WuDepartment of Integrated Medicine, The Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Xuemei HuangDepartment of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Yaqi KuangDepartment of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Zengmiao XingDepartment of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Xiujun DengDepartment of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Zuojie LuoDepartment of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Guangxi Medical University · CNTumor Hospital of Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThapsigargin (TG) is a natural product that exists in most parts of the plant

methodsIn this study, two human ACC cell lines including SW-13 and NCI-H295R were employed to explore the potential role of TG in ACC. A mouse xenograft model of SW-13 cells was established to verify the role of TG in vivo. The cell viability was tested using Cell Counting Kit-8 and Transwell assays. Flow cytometry and Hoechst 33,258 staining were employed to analyze cell apoptosis. RT-qPCR and Western blot (WB) were performed to explore the underlying mechanism of TG-induced apoptosis in ACC cells.

resultsThe results indicated that TG dose-dependently inhibited proliferation, migration and invasion in human ACC cells. TG significantly increased the mitochondrial rate of apoptosis and ER stress activity in ACC cells and suppressed ACC xenograft growth in vivo. In addition, the expression of Jun N-terminal kinase (JNK) signaling-related genes and proteins was upregulated by the treatment with TG.

conclusionOur findings suggest that TG inhibits the viability of ACC cells by inducing apoptosis through the activation of JNK signaling. Thus, TG is expected to be a potential candidate for the treatment of ACC.

Indexed as

Adrenal Cortex NeoplasmsAdrenocortical CarcinomaAnimalsAntineoplastic Agents, PhytogenicApoptosisBiological ProductsCell ProliferationCell SurvivalDrug Screening Assays, AntitumorEndoplasmic Reticulum StressHumansIn Vitro TechniquesJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Signaling SystemMiceAntineoplastic Agents, PhytogenicBiological ProductsJNK Mitogen-Activated Protein KinasesThapsigarginadrenocortical carcinomaapoptosisendoplasmic reticulum ER stressJun N-terminal kinase signalingthapsigargin

Identifiers

PMID31496655
PMCPMC6697672
OpenAlexW2967322438

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.