Evidence map›Paper›PMID 37750664›Full record

ArticleHistology and histopathology2024

Selenomethionine suppresses head and neck squamous cell carcinoma progression through TopBP1/ATR and TCAB1 signaling.

Bo Zhang, Xiaodong Wei, Jiwu Li

Abstract read
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In one paragraph

Article in Histology and histopathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

3 authors at 3 institutions in 1 country.

Bo Zhang *Hubei Provincial Key Laboratory of Occurrence and Intervention of Rheumatic Diseases, Hubei Minzu University, Enshi City, Hubei Province, China. zhboss1234@163.com.
Xiaodong Wei *Hubei Provincial Key Laboratory of Occurrence and Intervention of Rheumatic Diseases, Hubei Minzu University, Enshi City, Hubei Province, China.
Jiwu LiXiangya Stomatological Hospital and Xiangya School of Stomatology, Central South University, Changsha City, Hunan Province, China.
Central South University · CNHubei Provincial Center for Disease Control and Prevention · CNMinda Hospital · CN

Funding

Doctoral Startup fund of Hubei Minzu University MD2020B016Health Research Fund of Hubei Province WJ2019H142Key Projects of Enshi Science and Technology Plan D20220077Key Projects of Enshi Science and Technology Plan XYJ2020000059Natural Science Foundation of Hubei Province 2019CFB816Open Fund of Hubei Province Key Laboratory for Occurrence and Intervention of Rheumatic Diseases OIR20004AOpen Fund of Hubei Province Key Laboratory for Occurrence and Intervention of Rheumatic Diseases OIR20006AOpen Fund of Minda Hospital of Hubei Minzu University OIR202301Y
6 · The paper itself

Abstract

objectiveHead and neck squamous cell carcinoma (HNSCC) is a histological type of cancer originating from the head and neck. Selenium complexes have been considered as a potential treatment for HNSCC. Therefore, the present work focused on probing the mechanism of L-selenomethionine (SeMet) in HNSCC treatment.

methodsMTT and colony formation assays were carried out to analyze the survival rate and proliferation of HNSCC cells, respectively. TUNEL staining was performed to examine apoptosis of HNSCC cells. Additionally, qRT-PCR and Western blotting assays were performed to measure mRNA and protein levels, separately.

resultsSeMet treatment significantly hindered the survival and promoted the apoptosis of HNSCC cells in a dose- and time-dependently. SeMet administration promoted expression of TopBP1, ATR, H2AX, p-ATR and γ-H2AX, and suppressed that of TCAB1. Importantly, SeMet treatment suppressed the proliferation and facilitated the apoptosis of HNSCC cells, which were partly reversed by down-regulation of TopBP1 or up-regulation of TCAB1. The activation of SeMet to TopBP1/ATR signaling was rescued by TCAB1 up-regulating, and the inhibition of SeMet to TCAB1 expression was rescued by TopBP1 silencing.

conclusionOur findings show that SeMet inhibits the proliferation of HNSCC cells and promotes their apoptosis by targeting TopBP1/ATR and TCAB1 signaling. SeMet is a potential method for HNSCC treatment.

Indexed as

ApoptosisHead and Neck NeoplasmsSelenomethionineSignal TransductionSquamous Cell Carcinoma of Head and NeckAtaxia Telangiectasia Mutated ProteinsCarrier ProteinsCell Line, TumorCell ProliferationDisease ProgressionDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansNuclear ProteinsSelenium-Binding ProteinsAtaxia Telangiectasia Mutated ProteinsATR protein, humanCarrier ProteinsDNA-Binding ProteinsNuclear ProteinsSELENBP1 protein, humanSelenium-Binding ProteinsSelenomethionine

Identifiers

PMID37750664
OpenAlexW4387033175

What OpenQuestion holds

Textmetadata
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.