Evidence map›Paper›PMID 30317923›Full record

ArticleCell cycle (Georgetown, Tex.)2018

p27 inhibits CDK6/CCND1 complex formation resulting in cell cycle arrest and inhibition of cell proliferation.

Niannian Li, Jie Zeng, Fuze Sun, Xiaoling Tong, Gang Meng, Chunman Wu, Xin Ding, Lanlan Liu, Minjin Han, Cheng Lu and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-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

24 citing papers in PubMed, 42 citations in OpenAlex.

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  10. Therapeutic Potential of Targeting p27Archives of internal medicine research · 2024
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  13. Review
  14. Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021
    Review
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  18. Propofol activates AMPK to inhibit the growth of HepG2 cellsJournal of gastrointestinal oncology · 2020
    Article
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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 2 institutions in 1 country.

Niannian Lia State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Jie Zenga State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Fuze Suna State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Xiaoling Tonga State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Gang Menga State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Chunman Wua State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Xin Dinga State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Lanlan Liua State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Minjin Hana State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Cheng Lua State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Fangyin Daia State Key Laboratory of Silkworm Genome Biology, Key Laboratory of Sericultural Biology and Genetic Breeding, Ministry of Agriculture , College of Biotechnology, Southwest University , Chongqing , China.
Southwest University · CNState Key Laboratory of Silkworm Genomic Biology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p27 plays critical roles in cell proliferation, differentiation, and apoptosis, which have been well studied in mammals and Drosophila. However, the mechanisms underlying p27 regulation of the cell cycle have not been thoroughly researched. In this study, Genevestigator, Kaplan-Meier Plotter, and the Human Protein Atlas databases were used to analyze the expression of p27, cell division protein kinase 6 (CDK6), and cyclin D1 (CCND1), as well as its prognostic value in different tumor tissues and corresponding normal tissues. Quantitative PCR and immunohistochemistry were used to detect the expression of p27, CDK6, and CCND1 in the tissues of cancer patients. The effects of p27, CDK6, and CCND1 on the proliferation of lung cancer cells were examined by the MTT assay, and flow cytometry was used to investigate the mechanism by which p27 affected cell proliferation. Immunofluorescence, co-immunoprecipitation, and Western blotting were used to determine if p27 interacted with CDK and CCND1 to regulate the cell cycle. The results showed that p27, CDK6, and CCND1 played different roles in tumorigenesis and development, which are in accordance with CDK6 and CCND1 in affecting the cell cycle and cell proliferation. p27 regulated the cell cycle and inhibited cell proliferation by affecting formation of the cell cycle-dependent complex CDK6/CCND1, but did not directly affect the expression of CDK6 and CCND1. Moreover, CCND1 did not regulate the cell cycle alone, but rather, functioned together with CDK6. This study provides insights into the effects of p27 on tumor formation and development, and the underlying regulatory mechanisms.

Indexed as

Cell ProliferationA549 CellsAnimalsCell Cycle CheckpointsCyclin D1Cyclin-Dependent Kinase 6Cyclin-Dependent Kinase Inhibitor p27DrosophilaGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiceNeoplasmsProtein BindingCyclin D1Cyclin-Dependent Kinase 6Cyclin-Dependent Kinase Inhibitor p27CancerCCND1CDK6cell cyclecell proliferationp27

Identifiers

PMID30317923
PMCPMC6237435
OpenAlexW2897942487

What OpenQuestion holds

Textmetadata
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.