Evidence map›Paper›PMID 30461193›Full record

ArticleJournal of cellular and molecular medicine2019

Targeting PRMT5/Akt signalling axis prevents human lung cancer cell growth.

Shikui Zhang, Yaqiong Ma, Xiaoyan Hu, Yonghua Zheng, Xiaoke Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

46 citing papers in PubMed, 62 citations in OpenAlex.

  1. PRMT5 is a prognostic-related biomarker associated with the tumor immune microenvironment in lung adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

5 authors at 3 institutions in 1 country.

Shikui ZhangDepartment of Emergency, People's Hospital of Gansu Province, Lanzhou, China.
Yaqiong MaDepartment of Radiology, People's Hospital of Gansu Province, Lanzhou, China.
Xiaoyan HuDepartment of Respiratory Medicine, Shanghai Jinshan Tinglin Hospital, Shanghai, China.
Yonghua ZhengDepartment of Respiratory Medicine, Shanghai Jinshan Tinglin Hospital, Shanghai, China.ORCID 0000-0002-7799-9612
Xiaoke ChenDepartment of Thoracic Surgery, Shanghai Chest Hospital, Shanghai, China.
Gansu Provincial Hospital · CNJinshan Hospital of Fudan University · CNShanghai Chest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The emerging evidence reveals that protein arginine methyltransferase 5 (PRMT5) is involved in regulation of tumour cell proliferation and cancer development. Nevertheless, the exact role of PRMT5 in human lung cancer cell proliferation and the underlying molecular mechanism remains largely obscure. Here, we showed that PRMT5 was highly expressed in human lung cancer cells and lung cancer tissues. Furthermore, we generated PRMT5 stable knockdown cell lines (A549 and H1299 cells) and explored the functions of PRMT5 in lung cancer cell proliferation. We found that the down-regulation of PRMT5 by shRNA or the inhibition of PRMT5 by specific inhibitor GSK591 dramatically suppressed cyclin E1 and cyclin D1 expression and cell proliferation. Moreover, we uncovered that PRMT5 promoted lung cancer cell proliferation via regulation of Akt activation. PRMT5 was directly co-localized and interacted with Akt, but not PTEN and mTOR. Down-regulation or inhibition of PRMT5 markedly reduced Akt phosphorylation at Thr308 and Ser473, whereas the expression of PTEN and mTOR phosphorylation was unchanged, indicating that PRMT5 was an important upstream regulator of Akt and induced lung cancer cell proliferation. Altogether, our results indicate that PRMT5 promotes human lung cancer cell proliferation through direct interaction with Akt and regulation of Akt activity. Our findings also suggest that targeting PRMT5 may have therapeutic potential for treatment of human lung cancer.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinoma of LungApoptosisBiomarkers, TumorCell ProliferationCell Transformation, NeoplasticHumansLung NeoplasmsPrognosisProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRNA, Small InterferingSignal TransductionTOR Serine-Threonine KinasesTumor Cells, CulturedAKT1 protein, humanBiomarkers, TumorMTOR protein, humanPRMT5 protein, humanProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanRNA, Small InterferingTOR Serine-Threonine KinasesAktlung cancermTORPRMT5proliferationPTEN

Identifiers

PMID30461193
PMCPMC6349228
OpenAlexW2901706397

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.