Evidence map›Paper›PMID 35013447›Full record

ArticleScientific reports2022

The efficacy of PI3Kγ and EGFR inhibitors on the suppression of the characteristics of cancer stem cells.

Yanning Xu, Said M Afify, Juan Du, Bingbing Liu, Ghmkin Hassan, Qing Wang, Hanbo Li, Yixin Liu, Xiaoying Fu, Zhengmao Zhu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 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

12 authors at 4 institutions in 4 countries.

Yanning XuDepartment of Pathology, Tianjin Central Hospital of Gynecology Obstetrics, Nankai University Affiliated Maternity Hospital, Tianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, 300100, China.
Said M AfifyDepartment of Medical Bioengineering, Graduate School of Natural Science and Technology, Okayama University, Okayama, 700-8530, Japan.
Juan DuDepartment of Etiology, Shanxi Provincial Cancer Hospital, Taiyuan, 030013, China.
Bingbing LiuDepartment of Pathology, Tianjin Central Hospital of Gynecology Obstetrics, Nankai University Affiliated Maternity Hospital, Tianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, 300100, China.
Ghmkin HassanDepartment of Medical Bioengineering, Graduate School of Natural Science and Technology, Okayama University, Okayama, 700-8530, Japan.
Qing WangDepartment of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Hanbo LiDepartment of Pathology, Tianjin Central Hospital of Gynecology Obstetrics, Nankai University Affiliated Maternity Hospital, Tianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, 300100, China.
Yixin LiuDepartment of Pathology, Tianjin Central Hospital of Gynecology Obstetrics, Nankai University Affiliated Maternity Hospital, Tianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, 300100, China.
Xiaoying FuDepartment of Medical Bioengineering, Graduate School of Natural Science and Technology, Okayama University, Okayama, 700-8530, Japan.
Zhengmao ZhuDepartment of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Ling ChenDepartment of Pathology, Tianjin Central Hospital of Gynecology Obstetrics, Nankai University Affiliated Maternity Hospital, Tianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin, 300100, China. chenlingdoctor@126.com.
Masaharu SenoDepartment of Medical Bioengineering, Graduate School of Natural Science and Technology, Okayama University, Okayama, 700-8530, Japan. mseno@okayama-u.ac.jp.
Nankai University · CNOkayama University · JPTianjin Central Hospital of Gynecology Obstetrics · CNShanxi Provincial Cancer Hospital · CN

Funding

National Natural Science Foundation of China 81402320Natural Science Foundation of Tianjin, China 16JCYBJC27000the Open Fund of Tianjin Central Hospital of Gynecology Obstetrics / Tianjin Key Laboratory of human development and reproductive regulation 2019XH16the Open Fund of Tianjin Central Hospital of Gynecology Obstetrics / Tianjin Key Laboratory of human development and reproductive regulation 2019XH18
6 · The paper itself

Abstract

Cancer stem cells (CSCs) are capable of continuous proliferation, self-renewal and are proposed to play significant roles in oncogenesis, tumor growth, metastasis and cancer recurrence. We have established a model of CSCs that was originally developed from mouse induced pluripotent stem cells (miPSCs) by proposing miPSCs to the conditioned medium (CM) of cancer derived cells, which is a mimic of carcinoma microenvironment. Further research found that not only PI3K-Akt but also EGFR signaling pathway was activated during converting miPSCs into CSCs. In this study, we tried to observe both of PI3Kγ inhibitor Eganelisib and EGFR inhibitor Gefitinib antitumor effects on the models of CSCs derived from miPSCs (miPS-CSC) in vitro and in vivo. As the results, targeting these two pathways exhibited significant inhibition of cell proliferation, self-renewal, migration and invasion abilities in vitro. Both Eganelisib and Gefitinib showed antitumor effects in vivo while Eganelisib displayed more significant therapeutic efficacy and less side effects than Gefitinib on all miPS-CSC models. Thus, these data suggest that the inhibitiors of PI3K and EGFR, especially PI3Kγ, might be a promising therapeutic strategy against CSCs defeating cancer in the near future.

Indexed as

AnimalsApoptosisCell Line, TumorCell MovementCell ProliferationCell Self RenewalClass Ib Phosphatidylinositol 3-KinaseErbB ReceptorsFemaleGefitinibInduced Pluripotent Stem CellsMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessNeoplastic Stem CellsClass Ib Phosphatidylinositol 3-KinaseEGFR protein, mouseErbB ReceptorsGefitinibPhosphoinositide-3 Kinase InhibitorsPik3cg protein, mouseProtein Kinase Inhibitors

Identifiers

PMID35013447
PMCPMC8748513
OpenAlexW4205736113

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.