Evidence map›Paper›PMID 34094961›Full record

ArticleFrontiers in oncology2021

Selenite Induces Cell Cycle Arrest and Apoptosis

Zhen Cheng, Shuang Yu, Weiman He, Jie Li, Tianyi Xu, Junyu Xue, Peijie Shi, Shuwei Chen, Yanbing Li, Shubin Hong and 1 more

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 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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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

11 authors at 3 institutions in 1 country.

Zhen ChengDepartment of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Shuang YuDepartment of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Weiman HeDepartment of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Jie LiDepartment of Breast and Thyroid Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Tianyi XuZhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Junyu XueDepartment of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Peijie ShiDepartment of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Shuwei ChenDepartment of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.
Yanbing LiDepartment of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Shubin HongDepartment of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Haipeng XiaoDepartment of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyroid cancer is the most common endocrine malignancy, and its incidence has increased in the past decades. Selenium has been shown to have therapeutic effects against several tumors. However, its role in thyroid cancer and its underlying molecular mechanism remains to be explored. In the present study, we demonstrated that sodium selenite significantly decreased cell viability and induced G0/G1 cell cycle arrest and apoptosis in thyroid cancer cells in a dose-dependent manner. Transcriptomics revealed that sodium selenite induced intracellular reactive oxygen species (ROS) by promoting oxidative phosphorylation. Increased intracellular ROS levels inhibited the AKT/mTOR signaling pathway and upregulated EIF4EBP3. Intracellular ROS inhibition by N-acetylcysteine (NAC) ameliorated the cellular effects of sodium selenite. The

Indexed as

apoptosiscell cyclesodium selenitethe AKT/mTOR pathwaythyroid cancer (TC)

Identifiers

PMID34094961
PMCPMC8176115
OpenAlexW3165424217

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.