Evidence map›Paper›PMID 36032960›Full record

ArticlePeerJ2022

C1orf74 positively regulates the EGFR/AKT/mTORC1 signaling in lung adenocarcinoma cells.

Jinyong Guo, Aili Li, Ruolin Guo, Qiufeng He, Youru Wu, Yi Gou, Junfei Jin, Guojin Huang

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. 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.

Jinyong GuoLaboratory of Respiratory Diseases, The Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, P.R. China.
Aili LiLaboratory of Respiratory Diseases, The Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, P.R. China.
Ruolin GuoLaboratory of Respiratory Diseases, The Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, P.R. China.
Qiufeng HeLaboratory of Respiratory Diseases, The Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, P.R. China.
Youru WuLaboratory of Respiratory Diseases, The Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, P.R. China.
Yi GouLaboratory of Respiratory Diseases, The Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, P.R. China.
Junfei JinMolecular Medicine in Liver Injury and Repair, The Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Guojin HuangLaboratory of Respiratory Diseases, The Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, P.R. China.
Guilin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Lung adenocarcinoma (LUAD) is a major type of lung cancer with poor prognosis and low 5-year survival rate, which urgently needs further investigation in order to elucidate its mechanisms completely and discover novel therapeutic targets. C1orf74 is a novel protein with unknown function either in normal cells or cancer cells. The aim of this study is to investigate the expression and function of C1orf74 in LUAD cells. Methods: The expression of C1orf74 in LUAD was analyzed using the LUAD datasets from public databases. The prognostic value of C1orf74 in LUAD was analyzed using Kaplan-Meier Plotter. C1orf74 expression in LUAD cell line A549, H1993 and HCC827 was silenced using small interfering RNA, and then the effects of C1orf74 knockdown on proliferation, migration and invasion of LUAD cells were detected by colony formation assay and Transwell assay, the role of C1orf74 in EGFR/AKT/mTORC1 signaling pathway was examined by Western blot, and the function of C1orf74 in cell cycle was detected by flow cytometry. Results: The results of LUAD clinical data showed that C1orf74 was upregulated in LUAD tissues, and its high expression was associated with poor prognosis. The results from cultured LUAD cells demonstrated that C1orf74 knockdown inhibited cell proliferation, migration and invasion, but induced cell cycle arrest and autophagy. Moreover, C1orf74 knockdown suppressed EGFR/AKT/mTORC1 signaling in LUAD cells. In conclusion, the present study revealed that C1orf74 is upregulated in LUAD tissues and plays an oncogenic role in LUAD, and that C1orf74 positively regulates cell proliferation and mobility through the EGFR/AKT/mTORC1 signaling pathway in LUAD cells.

Indexed as

AdenocarcinomaAdenocarcinoma of LungLung NeoplasmsCell Line, TumorCell MovementErbB ReceptorsHumansMechanistic Target of Rapamycin Complex 1Proto-Oncogene Proteins c-aktSignal TransductionEGFR protein, humanErbB ReceptorsMechanistic Target of Rapamycin Complex 1Proto-Oncogene Proteins c-aktA549C1orf74EGFR/AKT/mTORC1 signalingH1993HCC827Lung adenocarcinoma

Identifiers

PMID36032960
PMCPMC9406791
OpenAlexW4292590117

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.