Evidence map›Paper›PMID 33742771›Full record

ArticleThoracic cancer2021

GPR12 inhibits migration and promotes apoptosis in esophageal cancer and hypopharyngeal cancer cells.

Minfa Zhang, Xiaoqi Yang, Shuai Chen, Wenming Jia, Xiaojie Ma, Juan Wang, Ye Qian, Dapeng Lei, Heng Liu, Xinliang Pan

Abstract read
In one paragraph

Article in Thoracic cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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.

Minfa ZhangDepartment of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, China.ORCID 0000-0002-2444-4461
Xiaoqi YangDepartment of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Shuai ChenDepartment of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Wenming JiaDepartment of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Xiaojie MaDepartment of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Juan WangDepartment of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Ye QianDepartment of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Dapeng LeiDepartment of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Heng LiuDepartment of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Xinliang PanDepartment of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, China.

Funding

Key Research and Development Projects of Shandong Province 2018GSF118029Key Research and Development Projects of Shandong Province 2019GSF108265Science and Technology Project of Jinan City 201805053Shandong Provincial Natural Science Foundation, China ZR2020MH280
6 · The paper itself

Abstract

backgroundG protein-coupled receptor 12 (GPR12) is an orphan receptor with no confirmed endogenous ligands. It plays important roles in both physiological and pathological conditions such as neurogenesis and neural inflammation. However, it remains unclear whether GPR12 regulates carcinogenesis and progression in head and neck squamous cell carcinoma (HNSCC), such as esophageal cancer (EC) and hypopharyngeal cancer (HC).

methodsThe Cancer Genome Atlas (TCGA) database was applied to explore the expression of GPR12. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of GPR12 in cancer tissues. Wound healing and transwell assays were carried out to verify the effect of GPR12 on cell migration. Flow cytometric analysis and caspase-Glo 3/7 assay were carried out to verify the influence of GPR12 on cell apoptosis. Western blotting was used to measure the expression of proteins related to migration and apoptosis.

resultThe qRT-PCR analyses showed that the expression of GPR12 decreased in EC and HC than that in their paired adjacent normal tissues. Wound healing assay and transwell assay demonstrated that GPR12 inhibited tumor cell migration. Flow cytometry analysis and Caspase-Glo 3/7 Assay suggested that GPR12 promoted apoptosis. The mechanism of GPR12 may function via modulating caspase-7, E-cadherin, and α-catenin in EC and HC cells.

conclusionIn conclusion, GPR12 induced apoptosis by activating caspase-7 and inhibited migration through epithelial-to-mesenchymal transition (EMT) in EC and HC. Our findings demonstrated that GPR12 as a potential tumor suppressor mediated cell migration and apoptosis in EC and HC.

Indexed as

ApoptosisCell MovementEsophageal NeoplasmsHumansHypopharyngeal NeoplasmsReceptors, G-Protein-CoupledTransfectionGPR12 protein, humanReceptors, G-Protein-CoupledApoptosisepithelial-to-mesenchymal transitionesophageal cancerGPR12; migration

Identifiers

PMID33742771
PMCPMC8107035

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.