Evidence map›Paper›PMID 34178653›Full record

ArticleFrontiers in oncology2021

The Anti-Non-Small Cell Lung Cancer Cell Activity by a mTOR Kinase Inhibitor PQR620.

Jian-Hua Zha, Ying-Chen Xia, Chun-Lin Ye, Zhi Hu, Qin Zhang, Han Xiao, Ben-Tong Yu, Wei-Hua Xu, Guo-Qiu Xu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 34 citations in OpenAlex.

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  15. SLC5A3 is important for cervical cancer cell growth.International journal of biological sciences · 2023
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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 5 institutions in 1 country.

Jian-Hua ZhaDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Ying-Chen XiaDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Chun-Lin YeDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Zhi HuDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Qin ZhangDepartment of Respiratory Medicine, Suzhou Hospital Affiliated Nanjing Medical University, Suzhou, China.
Han XiaoDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ben-Tong YuDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Wei-Hua XuDepartment of Cardiothoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Guo-Qiu XuDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, China.
First Affiliated Hospital of Nanchang University · CNNanchang University · CNHuazhong University of Science and Technology · CNSecond Affiliated Hospital of Soochow University · CNSuzhou Municipal Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In non-small-cell lung carcinoma (NSCLC), aberrant activation of mammalian target of rapamycin (mTOR) contributes to tumorigenesis and cancer progression. PQR620 is a novel and highly-potent mTOR kinase inhibitor. We here tested its potential activity in NSCLC cells. In primary human NSCLC cells and established cell lines (A549 and NCI-H1944), PQR620 inhibited cell growth, proliferation, and cell cycle progression, as well as cell migration and invasion, while inducing significant apoptosis activation. PQR620 disrupted assembles of mTOR complex 1 (mTOR-Raptor) and mTOR complex 2 (mTOR-Rictor-Sin1), and blocked Akt, S6K1, and S6 phosphorylations in NSCLC cells. Restoring Akt-mTOR activation by a constitutively-active Akt1 (S473D) only partially inhibited PQR620-induced cytotoxicity in NSCLC cells. PQR620 was yet cytotoxic in Akt1/2-silenced NSCLC cells, supporting the existence of Akt-mTOR-independent mechanisms. Indeed, PQR620 induced sphingosine kinase 1 (SphK1) inhibition, ceramide production and oxidative stress in primary NSCLC cells.

Indexed as

Aktmammalian target of rapamycinnon-small-cell lung carcinomaPQR620signalings

Identifiers

PMID34178653
PMCPMC8222575
OpenAlexW3169230476

What OpenQuestion holds

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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.