Evidence map›Paper›PMID 31605296›Full record

ArticleJournal of neuro-oncology2019

TRIM44 is indispensable for glioma cell proliferation and cell cycle progression through AKT/p21/p27 signaling pathway.

Xia Zhou, Yadong Yang, Pengcheng Ma, Na Wang, Dong Yang, Qiu Tu, Bin Sun, Tingxiu Xiang, Xudong Zhao, Zongliu Hou and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  9. Clinical Significance of TRIM44 Expression in Patients with Gastric Cancer.Asian Pacific journal of cancer prevention : APJCP · 2022
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  14. CMBs carrying PTX and CRISPR/Cas9 targetingMolecular medicine reports · 2021
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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

11 authors at 7 institutions in 1 country.

Xia ZhouKey Laboratory of Tumor Immunological Prevention and Treatment of Yunnan Province, Central Laboratory of Yan'an Hospital, Affiliated to Kunming Medical University, 245 East Ren Ming Road, Kunming, 650051, Yunnan, China.
Yadong YangCAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, No. 1 Beichen West Road, Chaoyang District, Beijing, 100101, China.
Pengcheng MaState Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China.
Na WangOncology and Hematology Department, Mianyang Hospital of T.C.M., Mianyang, 621000, Sichuan, China.
Dong YangKey Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, Yunnan, China.
Qiu TuKey Laboratory of Tumor Immunological Prevention and Treatment of Yunnan Province, Central Laboratory of Yan'an Hospital, Affiliated to Kunming Medical University, 245 East Ren Ming Road, Kunming, 650051, Yunnan, China.
Bin SunKey Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, Yunnan, China.
Tingxiu XiangChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xudong ZhaoKey Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, Yunnan, China.
Zongliu HouKey Laboratory of Tumor Immunological Prevention and Treatment of Yunnan Province, Central Laboratory of Yan'an Hospital, Affiliated to Kunming Medical University, 245 East Ren Ming Road, Kunming, 650051, Yunnan, China. HZL579@163.com.
Xiangdong FangCAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, No. 1 Beichen West Road, Chaoyang District, Beijing, 100101, China. fangxd@big.ac.cn.ORCID http://orcid.org/0000-0002-6628-8620
Kunming Institute of Zoology · CNBeijing Institute of Genomics · CNChinese Academy of Sciences · CNKunming Institute of Botany · CNKunming Medical University · CNSichuan Mianyang 404 Hospital · CNThe Affiliated Yongchuan Hospital of Chongqing Medical University · CN

Funding

Applied basic research projects of yunnan 2013FA020China Postdoctoral Science Foundation 2019M653500National Basic Research Program of China (973 Program) 2016YFC0901701National Basic Research Program of China (973 Program) 2017YFC0908402National Basic Research Program of China (973 Program) 2018YFC0910402National Basic Research Program of China (973 Program) 2018YFC0910702National Natural Science Foundation of China 81472862
6 · The paper itself

Abstract

purposeGlioma is one of the lethal cancers which needs effective therapeutic target. TRIM44 has been found playing a carcinogenic role in human tumors such as breast cancer and ovarian cancer. However, the pathophysiological significance of TRIM44 in glioma is still unclear.

methodsQuantitative-PCR and western blot were used to assess the expression of TRIM44 in glioma cells. For cell proliferation, Brdu incorporation and colony formation assays were performed. By Caspase 3 staining and FACS analysis, we revealed that TRIM44 knockdown induced glioma cell apoptosis. A BALB/c nude mouse xenograft model and following immunohistochemical (IHC) staining enables us to explore the effect of TRIM44 deletion on glioma growth in vivo. Western blot of p21, p27 and AKT indicated the possible role of TRIM44 in regulation AKT pathway in glioma.

resultsTRIM44 was significantly elevated in glioma cells, and high expression of TRIM44 is related to poor prognostic of glioma patients. TRIM44 knockdown by shRNAs inhibit glioma cell proliferation, migration, induced cell cycle disruption and further cellular apoptosis in vitro. As well, TRIM44 inactivation obviously inhibit tumor growth in xenograft model. Furthermore, the negative cell cycle regulators p21/p27 are significantly upregulated, while AKT which is known as the main regulator of p21/p27 is inactivated in TRIM44-dificient cells. These results suggested that TRIM44 inactivation disrupted cell cycle progression and inhibit cell proliferation through AKT/p21/p27 pathway in glioma.

conclusionTRIM44 was associated with oncogenic potential of glioma. Targeting TRIM44 might be beneficial for glioma therapy.

Indexed as

Signal TransductionAnimalsBrain NeoplasmsCell ProliferationCyclin-Dependent Kinase Inhibitor p21GliomaHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsMice, Inbred BALB CProto-Oncogene Proteins c-aktTripartite Motif ProteinsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Intracellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-aktTRIM44 protein, humanTripartite Motif ProteinsAKTCell cycleMigrationProliferationTRIM44

Identifiers

PMID31605296
OpenAlexW2979420822

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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.