Evidence map›Paper›PMID 32468683›Full record

ArticleJournal of cellular and molecular medicine2020

Plac8-mediated autophagy regulates nasopharyngeal carcinoma cell function via AKT/mTOR pathway.

Mao-Ling Huang, Cheng-Lin Qi, You Zou, Rui Yang, Yang Jiang, Jian-Fei Sheng, Yong-Gang Kong, Ze-Zhang Tao, Shi-Ming Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Genomewide CRISPR knockout screen identified PLAC8 as an essential factor for SADS-CoVs infection.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Multifaced roles of PLAC8 in cancer.Biomarker research · 2021
    Review
  17. Article
  18. 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

9 authors at 1 institution in 1 country.

Mao-Ling HuangDepartment of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Cheng-Lin QiDepartment of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
You ZouDepartment of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Rui YangDepartment of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Yang JiangDepartment of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Jian-Fei ShengDepartment of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Yong-Gang KongDepartment of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Ze-Zhang TaoDepartment of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Shi-Ming ChenDepartment of Otolaryngology-Head and Neck Surgery, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.ORCID 0000-0002-1216-004X
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To explore the relationship between autophagy and cell function, we investigated how PLAC8-mediated autophagy influences proliferation, apoptosis and epithelial-mesenchymal transition (EMT) in NPC. Colony formation analyses and CCK8 assays were used to assess the proliferative capacity of NPC cells. Transmission electron microscopy (TEM) was used to identify autophagosomes. Autophagic flux was monitored using the tandem monomeric RFP-GFP-tagged LC3 (tfLC3) assay. The rate of apoptosis in NPC cells was analysed by flow cytometry. Western blot analysis was used to evaluate the activation of autophagy and the signalling status of the AKT/mTOR pathway. Our study reveals that knocking out PLAC8 (koPLAC8) induces autophagy and apoptosis, while suppressing NPC cell proliferation and EMT. However, inhibition of autophagy with 3-methyladenine or by knocking down Beclin-1 reverses the cell proliferation, apoptosis and EMT influenced by koPLAC8. We find that koPLAC8 inhibits the phosphorylation of AKT and its downstream target, mTOR. Moreover, immunofluorescence and co-immunoprecipitation reveal complete PLAC8/AKT colocalization and PLAC8/AKT interaction, respectively. Furthermore, knockout of PLAC8 induced autophagy and inactivated AKT/mTOR signalling pathway of NPC xenografts. Overall, our findings demonstrate that koPLAC8 induces autophagy via the AKT/mTOR pathway, thereby inhibiting cell proliferation and EMT, and promoting apoptosis in NPC cells.

Indexed as

Signal TransductionAnimalsApoptosisAutophagyBeclin-1Cell Line, TumorCell ProliferationDisease Models, AnimalDisease SusceptibilityEpithelial-Mesenchymal TransitionGene Knockdown TechniquesHumansImmunohistochemistryMaleMiceModels, BiologicalBeclin-1PLAC8 protein, humanProteinsProto-Oncogene Proteins c-aktRNA, Small InterferingTOR Serine-Threonine KinasesAKT/mTOR pathwayapoptosisautophagyepithelial-mesenchymal transitionnasopharyngeal carcinomaplacenta specific 8 gene knockout

Identifiers

PMID32468683
PMCPMC7348153
OpenAlexW3029533420

What OpenQuestion holds

Textmetadata
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.