Evidence map›Paper›PMID 36428781›Full record

ArticleCancers2022

Girdin Promotes Tumorigenesis and Chemoresistance in Lung Adenocarcinoma by Interacting with PKM2.

Fuyang Cao, Desong Yang, Feiyu Tang, Can Lu, Xiang He, Songming Chen, Zhanghuan Yang, Siyuan Gong, Lunquan Sun, Atsushi Enomoto and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 14 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 3 institutions in 2 countries.

Fuyang CaoDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha 410008, China.ORCID 0000-0002-1096-268X
Desong YangHunan Clinical Medical Research Center of Accurate Diagnosis and Treatment for Esophageal Carcinoma, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410013, China.
Feiyu TangDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha 410008, China.
Can LuDepartment of Pathology, Xiangya Hospital, Central South University, Changsha 410008, China.
Xiang HeDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha 410008, China.
Songming ChenDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha 410008, China.
Zhanghuan YangDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha 410008, China.
Siyuan GongDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha 410008, China.
Lunquan SunDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha 410008, China.
Atsushi EnomotoDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.ORCID 0000-0002-9206-6116
Masahide TakahashiInternational Center for Cell and Gene Therapy, Fujita Health University, Toyoake 470-1192, Japan.
Liang WengDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha 410008, China.
Central South University · CNFujita Health University · JPNagoya University · JP

Funding

A scientific research project of Hunan Health Commission 202204022569Hunan Cancer Hospital Climb Plan ZX2020005Hunan Clinical Medical Research Center of Accurate Diagnosis and Treatment for Esophageal Carcinoma received by D.Y. 2020SK4005Hunan Provincial Natural Science Foundation of China 2022JJ30364National Natural Science Foundation of China 81974465;81900199The National Multidisciplinary Cooperative Diagnosis and Treatment Capacity Building Project for Major Diseases z027002The recruitment program for Huxiang Talents received by L.W. 2019RS1009
6 · The paper itself

Abstract

Girdin, an Akt substrate, has been reported to promote tumorigenesis in various tumors. However, the role of Girdin in a spontaneous tumor model has not yet been explored. Here, we studied the role of Girdin in lung adenocarcinoma (LUAD) using the autochthonous mouse model and found that Girdin led to LUAD progression and chemoresistance by enhancing the Warburg effect. Mechanistically, Girdin interacted with pyruvate kinase M2 (PKM2), which played a vital role in aerobic glycolysis. Furthermore, Girdin impaired Platelet Derived Growth Factor Receptor Beta (PDGFRβ) degradation, which in turn, promoted PKM2 tyrosine residue 105 (Y105) phosphorylation and inhibited PKM2 activity, subsequently promoting aerobic glycolysis in cancer cells. Taken together, our study demonstrates that Girdin is a crucial regulator of tumor growth and may be a potential therapeutic target for overcoming the resistance of LUAD cells to chemotherapy.

Indexed as

chemoresistanceGirdinLUADPKM2tumorigenesis

Identifiers

PMID36428781
PMCPMC9688487
OpenAlexW4309786498

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.