Evidence map›Paper›PMID 32086839›Full record

ArticleCancer science2020

Loss of the clock gene Per1 promotes oral squamous cell carcinoma progression via the AKT/mTOR pathway.

Guojun Yang, Yixin Yang, Hong Tang, Kai Yang

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Circadian rhythms and lung cancer biology and immunotherapy: Emerging opportunities and challenges.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review
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

4 authors at 1 institution in 1 country.

Guojun YangDepartment of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yixin YangDepartment of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Hong TangDepartment of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Kai YangDepartment of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID https://orcid.org/0000-0002-0884-3534
The Affiliated Yongchuan Hospital of Chongqing Medical University · CN

Funding

Natural Science Foundation of Chongqing, China cstc2018jcyjA0481
6 · The paper itself

Abstract

Current studies have shown that the clock gene Period 1 (Per1) is downregulated in various tumors and plays an important role in promoting tumor progression. However, the biological functions and mechanism of Per1 in tumors remain largely unknown. In this study, 86 specimens of oral squamous cell carcinoma (OSCC) tissues and adjacent noncancerous tissues were collected to determine the Per1 expression level and the clinical significance of Per1 expression. Per1 was stably inhibited or overexpressed in OSCC cells to investigate its function and mechanism in vitro and in vivo. We found that Per1 was remarkably downregulated in OSCC and that low Per1 expression was significantly associated with TNM clinical stage and poor prognosis of OSCC patients. Per1 overexpression in SCC15 OSCC cells (Per1-OE SCC15 cells) significantly promoted autophagy and apoptosis while inhibiting proliferation and the AKT/mTOR pathway. However, the results obtained in Per1-silenced TSCCA OSCC cells were opposite those obtained in Per1-OE SCC15 cells. After addition of the AKT activator SC79 to Per1-OE SCC15 cells, the increased autophagy and apoptosis as well as decreased proliferation were remarkably rescued. Furthermore, increased apoptosis was significantly rescued in Per1-OE SCC15 cells treated with the autophagy inhibitor autophinib. In vivo tumorigenicity assays also confirmed that Per1 overexpression suppressed tumor growth. Taken together, our findings demonstrate for the first time that Per1 promotes OSCC progression by inhibiting autophagy-mediated cell apoptosis and enhancing cell proliferation in an AKT/mTOR pathway-dependent manner, and Per1 could be used as a valuable therapeutic target for OSCC.

Indexed as

AdultAnimalsApoptosisAutophagyCarcinoma, Squamous CellCell Line, TumorCell ProliferationCell Transformation, NeoplasticDisease ProgressionFemaleGene ExpressionHumansMaleMiceMice, NudeMiddle AgedMTOR protein, humanPER1 protein, humanPeriod Circadian ProteinsProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasesautophagycarcinogenesisoral cancerperiod 1prognosis

Identifiers

PMID32086839
PMCPMC7226219
OpenAlexW3007445926

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.