Evidence map›Paper›PMID 35159102›Full record

ArticleCancers2022

ATP8B1 Knockdown Activated the Choline Metabolism Pathway and Induced High-Level Intracellular REDOX Homeostasis in Lung Squamous Cell Carcinoma.

Xiao Zhang, Rui Zhang, Pengpeng Liu, Runjiao Zhang, Junya Ning, Yingnan Ye, Wenwen Yu, Jinpu Yu

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

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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.

Xiao ZhangCancer Molecular Diagnostics Core, National Clinical Research Center of Caner, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin Medical University Cancer Institute & Hospital, Tianjin 300060, China.
Rui ZhangCancer Molecular Diagnostics Core, National Clinical Research Center of Caner, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin Medical University Cancer Institute & Hospital, Tianjin 300060, China.
Pengpeng LiuCancer Molecular Diagnostics Core, National Clinical Research Center of Caner, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin Medical University Cancer Institute & Hospital, Tianjin 300060, China.
Runjiao ZhangCancer Molecular Diagnostics Core, National Clinical Research Center of Caner, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin Medical University Cancer Institute & Hospital, Tianjin 300060, China.
Junya NingCancer Molecular Diagnostics Core, National Clinical Research Center of Caner, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin Medical University Cancer Institute & Hospital, Tianjin 300060, China.
Yingnan YeCancer Molecular Diagnostics Core, National Clinical Research Center of Caner, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin Medical University Cancer Institute & Hospital, Tianjin 300060, China.
Wenwen YuNational Clinical Research Center of Caner, Tianjin's Clinical Research Center for Cancer, Key Laboratory of Cancer Immunology and Biotherapy, Department of Immunology, Tianjin Medical University Cancer Institute & Hospital, Tianjin 300060, China.
Jinpu YuCancer Molecular Diagnostics Core, National Clinical Research Center of Caner, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin Medical University Cancer Institute & Hospital, Tianjin 300060, China.
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

National Natural Science Foundation of China 82173198 and 82072588National Science and Technology Support Program of China 2018ZX09201015Project of Graduate research innovation of Tianjin 2020YJSB166Project of Science and Technology of Tianjin 18JCQNJC82700
6 · The paper itself

Abstract

The flippase ATPase class I type 8b member 1 (ATP8B1) is essential for maintaining the stability and polarity of the epithelial membrane and can translocate specific phospholipids from the outer membrane to the inner membrane of the cell. Although ATP8B1 plays important roles in cell functions, ATP8B1 has been poorly studied in tumors and its prognostic value in patients with lung squamous cell carcinoma (LUSC) remains unclear. By investigating the whole genomic expression profiles of LUSC samples from The Cancer Genome Atlas (TCGA) database and Tianjin Medical University Cancer Institute and Hospital (TJMUCH) cohort, we found that low expression of ATP8B1 was associated with poor prognosis of LUSC patients. The results from cellular experiments and a xenograft-bearing mice model indicated that ATP8B1 knockdown firstly induced mitochondrial dysfunction and promoted ROS production. Secondly, ATP8B1 knockdown promoted glutathione synthesis via upregulation of the CHKA-dependent choline metabolism pathway, therefore producing and maintaining high-level intracellular REDOX homeostasis to aggravate carcinogenesis and progression of LUSC. In summary, we proposed ATP8B1 as a novel predictive biomarker in LUSC and targeting ATP8B1-driven specific metabolic disorder might be a promising therapeutic strategy for LUSC.

Indexed as

ATP8B1CHKALUSCREDOX

Identifiers

PMID35159102
PMCPMC8834475
OpenAlexW4210903306

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.