Evidence map›Paper›PMID 34997428›Full record

ArticleMolecular biology reports2022

G-protein coupled receptor 34 regulates the proliferation and growth of LS174T cells through differential expression of PI3K subunits and PTEN.

Bo Zuo, Na Wu, Shen Yang, Zhaohui Zhong, Mei Li, Xin Yu, Yulan Liu, Weidong Yu

Open access · hybridAbstract read
In one paragraph

Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Cryo-EM structures of human GPR34 enable the identification of selective antagonists.Proceedings of the National Academy of Sciences of the United States of America · 2023
    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

8 authors at 1 institution in 1 country.

Bo Zuo *Department of Central Laboratory & Institute of Clinical Molecular Biology, Peking University People's Hospital, Beijing, 100044, People's Republic of China.
Na Wu *Department of Central Laboratory & Institute of Clinical Molecular Biology, Peking University People's Hospital, Beijing, 100044, People's Republic of China.
Shen Yang *Department of General Surgery, Peking University People's Hospital, Beijing, 100044, People's Republic of China.
Zhaohui ZhongDepartment of General Surgery, Peking University People's Hospital, Beijing, 100044, People's Republic of China.
Mei LiDepartment of Central Laboratory & Institute of Clinical Molecular Biology, Peking University People's Hospital, Beijing, 100044, People's Republic of China.
Xin YuDepartment of Hepatobiliary Surgery, Peking University People's Hospital, Beijing, 100044, People's Republic of China.
Yulan LiuDepartment of Gastroenterology, Peking University People's Hospital, Beijing, 100044, People's Republic of China.
Weidong YuDepartment of Central Laboratory & Institute of Clinical Molecular Biology, Peking University People's Hospital, Beijing, 100044, People's Republic of China. weidongyu@bjmu.edu.cn.ORCID http://orcid.org/0000-0002-7573-4979
Peking University · CN

Funding

National Natural Science Foundation of China 30872923National Natural Science Foundation of China 32070116National Natural Science Foundation of China 81672853National Natural Science Foundation of China 82000328Natural Science Foundation of Jilin Province 31500098Peking University People's Hospital Research and Development Foundation RDH2020-11
6 · The paper itself

Abstract

purposeG-protein coupled receptor (GPR 34) has been found to play important roles in some cancers and regulates the proliferation, apoptosis, and migration of these cancer cells. However, the mechanisms underlying how GPR34 functions to regulate growth and proliferation of colorectal cancer cells remains to be clarified.

methodsWe employed stable GPR34 knockdown LS174T cell models, GPR34 Mab blocking, a CCK-8 kit, and a colony formation assay to characterize the effect of GPR34 on the proliferation of LS174T in vitro and xenograft tumor growth in vivo. The mRNA level of GPR34 was detected by RT-PCR in tumor tissues and adjacent normal tissues from 34 CRC patients.

resultsBased on RT-PCR results, GPR34 exhibited high level in tumor samples compared with adjacent normal samples. Increased expression of GPR34 is more associated with poor prognosis of CRC as shown in The Cancer Genome Atlas (TCGA) dataset by Kaplan-Meier survival analysis. Furthermore, we showed that GPR34 knockdown inhibited the proliferation of LS174T colon cancer cells and related xenograft tumor growth. Searching for the distinct molecular mechanism, we identified several contributors to proliferation of LS174T colon cancer cells: PI3K subunits/PTEN, PDK1/AKT, and Src/Raf/Ras/ERK. GPR34 knockdown inhibited the proliferation of LS174T cells by upregulating expression of PTEN, and downregulating expression of PI3K subunits p110-beta.

conclusionOur findings provide direct evidence that GPR34 regulates the proliferation of LS174T cells and the growth of LS174T tumor xenografts by regulating different pathways. High expression of GPR34 mRNA could then be used to predict poor prognosis of CRC.

Indexed as

Colorectal NeoplasmsPhosphatidylinositol 3-KinasesReceptors, LysophospholipidApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionG-protein-coupled receptor 34Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseReceptors, LysophospholipidColorectal cancerGPR34PI3K subunitsProliferationXenograft tumor growth

Identifiers

PMID34997428
PMCPMC8924081
OpenAlexW4205891291

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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.