Evidence map›Paper›PMID 34452627›Full record

ArticleJournal of experimental & clinical cancer research : CR2021

Cyclin G2 reverses immunosuppressive tumor microenvironment and potentiates PD-1 blockade in glioma.

Sen Li, Chenyang Zhao, Jinlan Gao, Xinbin Zhuang, Shuang Liu, Xuesha Xing, Qi Liu, Chen Chen, Shusen Wang, Yang Luo

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. 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

10 authors at 1 institution in 1 country.

Sen LiThe Research Center for Medical Genomics, Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Science, China Medical University, No.77 Puhe Road, Shenyang North New Area, Liaoning Province, Shenyang, People's Republic of China.
Chenyang ZhaoThe Research Center for Medical Genomics, Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Science, China Medical University, No.77 Puhe Road, Shenyang North New Area, Liaoning Province, Shenyang, People's Republic of China.
Jinlan GaoThe Research Center for Medical Genomics, Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Science, China Medical University, No.77 Puhe Road, Shenyang North New Area, Liaoning Province, Shenyang, People's Republic of China.
Xinbin ZhuangThe Research Center for Medical Genomics, Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Science, China Medical University, No.77 Puhe Road, Shenyang North New Area, Liaoning Province, Shenyang, People's Republic of China.
Shuang LiuThe Research Center for Medical Genomics, Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Science, China Medical University, No.77 Puhe Road, Shenyang North New Area, Liaoning Province, Shenyang, People's Republic of China.
Xuesha XingThe Research Center for Medical Genomics, Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Science, China Medical University, No.77 Puhe Road, Shenyang North New Area, Liaoning Province, Shenyang, People's Republic of China.
Qi LiuThe Research Center for Medical Genomics, Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Science, China Medical University, No.77 Puhe Road, Shenyang North New Area, Liaoning Province, Shenyang, People's Republic of China.
Chen ChenThe Research Center for Medical Genomics, Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Science, China Medical University, No.77 Puhe Road, Shenyang North New Area, Liaoning Province, Shenyang, People's Republic of China.
Shusen WangThe Research Center for Medical Genomics, Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Science, China Medical University, No.77 Puhe Road, Shenyang North New Area, Liaoning Province, Shenyang, People's Republic of China.
Yang LuoThe Research Center for Medical Genomics, Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Science, China Medical University, No.77 Puhe Road, Shenyang North New Area, Liaoning Province, Shenyang, People's Republic of China. yluo@cmu.edu.cn.
China Medical University · CN

Funding

Foundation of Liaoning Province Education Administration (CN) JC2019031National Natural Science Foundation of China No.82070794Natural Science Foundation of Liaoning Province No.2019-BS-285
6 · The paper itself

Abstract

backgroundExpression of aberrant cyclin G2 is a key factor contributing to cancer biological processes, including glioma. However, the potential underlying mechanisms of cyclin G2 in the glioma tumor immune microenvironment remain unclear.

methodsCo-immunoprecipitation (co-IP), in situ proximity ligation assay (PLA), and in vitro kinase assay were conducted to reveal the underlying mechanism by which cyclin G2 regulates Y10 phosphorylation of LDHA. Further, the biological roles of cyclin G2 in cell proliferation, migration, invasion capacity, apoptosis, glycolysis, and immunomodulation were assessed through in vitro and in vivo functional experiments. Expressions of cyclin G2 and Foxp3 in glioma specimens was determined by immunohistochemistry.

resultsIn this study, we found that cyclin G2 impeded the interaction between LDHA and FGFR1, thereby decreasing Y10 phosphorylation of LDHA through FGFR1 catalysis. Cyclin G2 inhibited proliferation, migration, invasion capacity, and glycolysis and promoted apoptosis glioma cells via suppressing Y10 phosphorylation of LDHA. Moreover, we further verified that cyclin G2 reversed the immunosuppressive to antitumor immune microenvironment through inhibiting lactate production by glioma cells. Besides, cyclin G2 potentiated PD-1 blockade and exerted strong antitumor immunity in the glioma-bearing mice model.

conclusionsCyclin G2 acts as a potent tumor suppressor in glioma and enhances responses to immunotherapy. Our findings may be helpful in selecting glioma patients for immunotherapy trials in the future.

Indexed as

AnimalsApoptosisBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationCyclin G2GliomaGlycolysisHumansMiceMice, Inbred C57BLNeoplasm InvasivenessNF-kappa BPhosphorylationProgrammed Cell Death 1 ReceptorCCNG2 protein, humanCyclin G2NF-kappa BPDCD1 protein, humanProgrammed Cell Death 1 ReceptorCyclin G2GliomaImmunosuppressive microenvironmentLDHAPD-1

Identifiers

PMID34452627
PMCPMC8400712
OpenAlexW3194172126

What OpenQuestion holds

Textmetadata
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.