Evidence map›Paper›PMID 36759724›Full record

ArticleBritish journal of cancer2023

Sec61γ is a vital protein in the endoplasmic reticulum membrane promoting tumor metastasis and invasion in lung adenocarcinoma.

Shanqi Xu, Xin Li, Jianxiong Geng, Yingyue Cao, Yan Yu, Lishuang Qi

Abstract read
In one paragraph

Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. SEC61G assistsProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Review
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

6 authors.

Shanqi Xu *Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Xin Li *College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Jianxiong GengDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Yingyue CaoDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Yan YuDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China. yuyan@hrbmu.edu.cn.ORCID http://orcid.org/0000-0002-8840-9497
Lishuang QiCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China. qilishuang7@ems.hrbmu.edu.cn.ORCID http://orcid.org/0000-0002-2991-6544

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is one of the most common malignant tumors worldwide. Finding effective prognostic markers and therapeutic targets is of great significance for controlling metastasis and invasion clinically.

methodsThe open copy-number aberrations and gene expression datasets were analysed, and the data of 102 LUAD patients was used for further validation. The cell proliferation, colony formation, migration, invasion assays and mice tumor models were used to detect the function of SEC61G. The epidermal growth factor receptor (EGFR) pathway was also detected to find the mechanism of Sec61γ.

resultsBased on the open datasets, we found that the high level of SEC61G mRNA may drive LUAD metastasis. Furthermore, the overexpression of Sec61γ protein was significantly associated with poor prognosis and greater tumor cell proliferation and metastasis. The SEC61G knockdown could inhibit the EGFR pathway, including STAT3, AKT and PI3K, which can be reversed by Sec61γ overexpression and epithelial growth factor (EGF) supplement.

conclusionsSec61γ promoted the proliferation, metastasis, and invasion of LUAD through EGFR pathways. Sec61γ might be a potential target for the treatment of LUAD metastases.

Indexed as

AdenocarcinomaAdenocarcinoma of LungLung NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationEndoplasmic ReticulumErbB ReceptorsGene Expression Regulation, NeoplasticMiceErbB Receptors

Identifiers

PMID36759724
PMCPMC10070493

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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.