Evidence map›Paper›PMID 36278918›Full record

ArticleJournal of the Chinese Medical Association : JCMA2022

PER3 plays anticancer roles in the oncogenesis and progression of breast cancer via regulating MEK/ERK signaling pathway.

Yinfeng Liu, Zizheng Wu, Yanli Li, Jing Zhang, Yang Gao, Guanli Yuan, Meng Han

Open access · hybridAbstract read
In one paragraph

Article in Journal of the Chinese Medical Association : JCMA, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Circadian clock and cancer.Military Medical Research · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Circadian geneOpen life sciences · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Biological clock regulation by theFrontiers in cell and developmental biology · 2024
    Review
  14. 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

7 authors at 1 institution in 1 country.

Yinfeng LiuDepartment of Breast Surgery, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei, China.
Zizheng WuDepartment of Breast Surgery, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei, China.
Yanli LiDepartment of Orthopedics, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei, China.
Jing ZhangDepartment of Orthopedics, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei, China.
Yang GaoDepartment of Intensive Care Unit, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei, China.
Guanli YuanDepartment of Respiratory and Critical Care Medicine, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei, China.
Meng HanDepartment of Breast Surgery, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei, China.
First Hospital of Qinhuangdao · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe study aimed at exploring the expression of period circadian regulator 3 (PER3), a major member of the circadian clock gene family, and its biological function in breast cancer.

methodsPER3-silencing and PER3-overexpression cell lines were established by transfecting with pGenesil1-PER3 and Lenti-blast-PER3 vector, respectively.

resultsThe results showed that the expression of PER3 was downregulated in breast cancer tissues and cell lines ( p < 0.001), and its low expression was significantly correlated with advanced tumor stage ( p = 0.031) and advanced T stage ( p = 0.018). Cell functional experiments indicated that the silencing of PER3 elevated the ability of breast cancer cells to proliferate, invade, and metastasize in vitro ( p < 0.05), whereas overexpression of PER3 had an inhibitory effect on these malignant phenotype of breast cancer cells ( p < 0.05). Moreover, the activation of MEK/ERK signaling pathway was evidently inhibited by silencing of PER3, as evidenced by decreased expression levels of p-MEK and p-ERK1/2 proteins in breast cancer cells ( p < 0.05). PER3-silencing and PER3-overexpression cells were treated with PD98059 (an inhibitor of MEK/ERK signaling) and TPA (an activator of MEK/ERK signaling), respectively. It was observed that PER3 silencing-mediated malignant phenotype in breast cancer cells was markedly suppressed by PD98059 treatment. Instead, TPA exposure reversed the inhibitory effects of PER3 overexpression on DNA synthesis, proliferation, migration, and invasion of breast cancer cells.

conclusionThese findings suggested that PER3 function as a tumor suppressor in the development and progression of breast cancer and its anticancer roles might be dependent on the MEK/ERK signaling pathway.

Indexed as

Breast NeoplasmsCarcinogenesisMAP Kinase Signaling SystemPeriod Circadian ProteinsCell Line, TumorCell ProliferationFemaleHumansMitogen-Activated Protein Kinase KinasesSignal TransductionMitogen-Activated Protein Kinase KinasesPER3 protein, humanPeriod Circadian Proteins

Identifiers

PMID36278918
PMCPMC12755356
OpenAlexW4307179395

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.