Evidence map›Paper›PMID 34568067›Full record

ArticleFrontiers in oncology2021

ASF1B Promotes Oncogenesis in Lung Adenocarcinoma and Other Cancer Types.

Wencheng Zhang, Zhouyong Gao, Mingxiu Guan, Ning Liu, Fanjie Meng, Guangshun Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

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  11. The interaction betweenAnnals of medicine · 2023
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  12. Bioinformatics Analysis and Screening of Potential Target Genes Related to the Lung Cancer Prognosis.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2023
    Article
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  15. Review
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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

6 authors at 1 institution in 1 country.

Wencheng ZhangDepartment of Oncology, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin, China.
Zhouyong GaoDepartment of Thoracic Surgery, Baodi Clinical College of Tianjin Medical University, Tianjin, China.
Mingxiu GuanDepartment of Laboratory, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin, China.
Ning LiuDepartment of Pathology, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin, China.
Fanjie MengDepartment of Thoracic Surgery, The Second Hospital of Tianjin Medical University, Tianjin, China.
Guangshun WangDepartment of Oncology, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin, China.
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-silencing function 1B histone chaperone (ASF1B) is known to be an important modulator of oncogenic processes, yet its role in lung adenocarcinoma (LUAD) remains to be defined. In this study, an integrated assessment of The Cancer Genome Atlas (TCGA) and genotype-tissue expression (GTEx) datasets revealed the overexpression of ASF1B in all analyzed cancer types other than LAML. Genetic, epigenetic, microsatellite instability (MSI), and tumor mutational burden (TMB) analysis showed that ASF1B was regulated by single or multiple factors. Kaplan-Meier survival curves suggested that elevated ASF1B expression was associated with better or worse survival in a cancer type-dependent manner. The CIBERSORT algorithm was used to evaluate immune microenvironment composition, and distinct correlations between ASF1B expression and immune cell infiltration were evident when comparing tumor and normal tissue samples. Gene set enrichment analysis (GSEA) indicated that ASF1B was associated with proliferation- and immunity-related pathways. Knocking down ASF1B impaired the proliferation, affected cell cycle distribution, and induced cell apoptosis in LUAD cell lines. In contrast, ASF1B overexpression had no impact on the malignant characteristics of LUAD cells. At the mechanistic level, ASF1B served as an indirect regulator of DNA Polymerase Epsilon 3, Accessory Subunit (POLE3), CDC28 protein kinase regulatory subunit 1(CKS1B), Dihydrofolate reductase (DHFR), as established through proteomic profiling and Immunoprecipitation-Mass Spectrometry (IP-MS) analyses. Overall, these data suggested that ASF1B serves as a tumor promoter and potential target for cancer therapy and provided us with clues to better understand the importance of ASF1B in many types of cancer.

Indexed as

ASF1Bimmune infiltration cellslung adenocarcinomaprofilingprognosis

Identifiers

PMID34568067
PMCPMC8459715
OpenAlexW3201368671

What OpenQuestion holds

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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.