Evidence map›Paper›PMID 36050267›Full record

ArticleClinical and experimental pharmacology & physiology2022

PD-L1/PD-L1 signalling promotes colorectal cancer cell migration ability through RAS/MEK/ERK.

Yihui Cao, Weiye Liang, Lian Fang, Ming-Kai Liu, Jia Zuo, Ying-Long Peng, Jia-Jie Shan, Rui-Xia Sun, Jie Zhao, Jian Wang

Open access · hybridAbstract read
In one paragraph

Article in Clinical and experimental pharmacology & physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.1field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. 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

10 authors at 2 institutions in 1 country.

Yihui Cao *School of Biology and Biological Engineering, South China University of Technology, Guangzhou, China.
Weiye Liang *Department of Neurobiology, School of Medicine, South China University of Technology, Guangzhou, China.ORCID 0000-0002-2164-4791
Lian Fang *Department of Neurobiology, School of Medicine, South China University of Technology, Guangzhou, China.
Ming-Kai LiuDepartment of Neurobiology, School of Medicine, South China University of Technology, Guangzhou, China.
Jia ZuoDepartment of Neurobiology, School of Medicine, South China University of Technology, Guangzhou, China.
Ying-Long PengDepartment of Neurobiology, School of Medicine, South China University of Technology, Guangzhou, China.
Jia-Jie ShanDepartment of Neurobiology, School of Medicine, South China University of Technology, Guangzhou, China.
Rui-Xia SunBioscience Laboratory, BIOS bioscience and Technology Limited Company, Guangzhou, China.
Jie ZhaoDepartment of Neurobiology, School of Medicine, South China University of Technology, Guangzhou, China.
Jian WangSchool of Biology and Biological Engineering, South China University of Technology, Guangzhou, China.ORCID 0000-0003-1441-8312
South China University of Technology · CNBioscience (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Programmed death ligand 1 (PD-L1) is widely known as an immune checkpoint, and immunotherapy through the inhibition of checkpoint molecules has become an important component in the successful treatment of tumours via programmed death 1 (PD-1)/PD-L1 signalling pathways. However, its biological functions and expression profile in colorectal cancer (CRC) are elusive. We previously found that PD-L1 can bind to PD-L1 and cause cell detachment. However, the detailed molecular mechanisms of how PD-L1 binds to PD-L1 and how it transmits signals to the cell remain unclear. In this study, we disclosed that PD-L1 expression was dramatically upregulated in CRC compared to normal tissues. Ectopic expression of PD-L1 inhibits cell adhesive capacity and promotes cell migration in CRC cell lines, while silencing PD-L1 had the opposite effects and suppressed invasion and proliferation. Mechanistically, PD-L1 was found to promote epithelial-mesenchymal transition (EMT) through the ERK signalling molecule pathway and interacted with the 1-86 aa fragment of KRAS to transduce signals. Collectively, our study demonstrated the role of PD-L1 after binding to PD-L1 in CRC, thereby providing a new theoretical basis for further improving immunotherapy with anti-PD-L1 antibodies.

Indexed as

B7-H1 AntigenColorectal NeoplasmsCell MovementExtracellular Signal-Regulated MAP KinasesHumansMitogen-Activated Protein Kinase Kinasesras ProteinsSignal TransductionB7-H1 AntigenExtracellular Signal-Regulated MAP KinasesMitogen-Activated Protein Kinase Kinasesras Proteinscell adhesioncolorectal cancer (CRC)ERKKRASmigrationPD-L1

Identifiers

PMID36050267
PMCPMC9826327
OpenAlexW4294132531

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.