Evidence map›Paper›PMID 35082393›Full record

ArticleActa pharmacologica Sinica2022

ACT001 inhibits pituitary tumor growth by inducing autophagic cell death via MEK4/MAPK pathway.

Lin Cai, Ze-Rui Wu, Lei Cao, Jia-Dong Xu, Jiang-Long Lu, Cheng-de Wang, Jing-Hao Jin, Zhe-Bao Wu, Zhi-Peng Su

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 16 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

9 authors at 4 institutions in 1 country.

Lin Cai *Department of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Ze-Rui Wu *Department of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Lei Cao *Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.
Jia-Dong XuDepartment of Cardio‑Thoracic Surgery, Zhoushan Hospital, Zhoushan, 316021, China.
Jiang-Long LuDepartment of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Cheng-de WangDepartment of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Jing-Hao JinDepartment of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Zhe-Bao WuDepartment of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. zhebaowu@aliyun.com.
Zhi-Peng SuDepartment of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. drsuzhipeng@163.com.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CNCapital Medical University · CNZhoushan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ACT001, derived from traditional herbal medicine, is a novel compound with effective anticancer activity in clinical trials. However, little is known regarding its role in pituitary adenomas. Here, we demonstrated that ACT001 suppressed cell proliferation and induced cell death of pituitary tumor cells in vitro and in vivo. ACT001 was also effective in suppressing the growth of different subtypes of human pituitary adenomas. The cytotoxic mechanism ACT001 employed was mainly related to autophagic cell death (ACD), indicated by autophagosome formation and LC3-II accumulation. In addition, ACT001-mediated inhibitory effect decreased when either ATG7 was downregulated or cells were cotreated with autophagy inhibitor 3-methyladenine (3-MA). RNA-seq analysis showed that mitogen-activated protein kinase (MAPK) pathway was a putative target of ACT001. Specifically, ACT001 treatment promoted the phosphorylation of JNK and P38 by binding to mitogen-activated protein kinase kinase 4 (MEK4). Our study indicated that ACT001-induced ACD of pituitary tumor cells via activating JNK and P38 phosphorylation by binding with MEK4, and it might be a novel and effective anticancer drug for pituitary adenomas.

Indexed as

Antineoplastic AgentsAutophagic Cell DeathPituitary NeoplasmsApoptosisAutophagyCell Line, TumorFuransHumansMAP Kinase Kinase 4MAP Kinase Signaling SystemMitogen-Activated Protein KinasesACT001Antineoplastic AgentsFuransMAP2K4 protein, humanMAP Kinase Kinase 4Mitogen-Activated Protein KinasesACT001autophagic cell deathJNKMEK4P38pituitary adenoma

Identifiers

PMID35082393
PMCPMC9433416
OpenAlexW4210663722

What OpenQuestion holds

Textmetadata
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.