Evidence map›Paper›PMID 41887693›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2026

[Selenocystine inhibits colon cancer cell growth by promoting reactive oxygen species generation to trigger oxidative damage].

Qile Song, Yikai Miao, Xiaotong Feng, Yifan Wang, Wei Liu, Qi Wei, Xinru Yu, Wenwen Chen, Xiaoyan Fu

Abstract readEnglish Abstract
PubMed Full text at PMC Publisher
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Qile SongDepartment of Neurology, Shandong Provincial Key Laboratory of Brain Injury and Functional Rehabilitation, Second Affiliated Hospital of Shandong First Medical University, Taian 271000, China.
Yikai MiaoPostgraduate Training Base of Linyi People's Hospital of Shandong Province, Guangzhou University of Chinese Medicine, Guangzhou 510000, China.
Xiaotong FengDepartment of Neurology, Shandong Provincial Key Laboratory of Brain Injury and Functional Rehabilitation, Second Affiliated Hospital of Shandong First Medical University, Taian 271000, China.
Yifan WangDepartment of Neurology, Shandong Provincial Key Laboratory of Brain Injury and Functional Rehabilitation, Second Affiliated Hospital of Shandong First Medical University, Taian 271000, China.
Wei LiuDepartment of Neurology, Shandong Provincial Key Laboratory of Brain Injury and Functional Rehabilitation, Second Affiliated Hospital of Shandong First Medical University, Taian 271000, China.
Qi WeiDepartment of Neurology, Shandong Provincial Key Laboratory of Brain Injury and Functional Rehabilitation, Second Affiliated Hospital of Shandong First Medical University, Taian 271000, China.
Xinru YuDepartment of Neurology, Shandong Provincial Key Laboratory of Brain Injury and Functional Rehabilitation, Second Affiliated Hospital of Shandong First Medical University, Taian 271000, China.
Wenwen ChenDepartment of Pharmacy, Second Affiliated Hospital.
Xiaoyan FuSchool of Clinic and Basic Medicine, Shandong First Medical University, Taian 271000, China.

Funding

National Natural Science Foundation of China 81701178
6 · The paper itself

Abstract

objectivesTo explore the molecular mechanism by which selenocystine (SeC) inhibits colon cancer cell growth

methodsColon cancer cells (RKO, HCT-116, and LoVo) were cultured and treated with 5, 10, or 20 μmol/L SeC for 24 h and 48 h. MTT assay was used to detect the cell viability, and wound healing assay was used to examine changes in cell migration. Flow cytometry with PI staining was used to analyze cell cycle arrest and apoptosis. Fluorescence probes were employed to monitor reactive oxygen species (ROS) generation, mitochondrial morphology and membrane potential, and the changes in ferroptosis were evaluated by detecting malondialdehyde (MDA), glutathione (GSH) and ferrous ion (Fe

resultsSeC at all the 3 doses significantly inhibited proliferation and migration of colon cancer cells, down-regulated the expression of cell cycle-related proteins CDK2 and CDK4 and activated the apoptotic proteins PARP and caspase-9. Western blotting showed that SeC decreased the expression of ferroptosis proteins FTH1 and xCT and increased the expression of DMT1. The levels of MDA and Fe

conclusionsSeC induces apoptosis and ferroptosis of colon cancer cells by promoting ROS generation and initiating oxidative damage, suggesting the potential of SeC as a potential chemotherapeutic agent for colon cancer.

Indexed as

Colonic NeoplasmsCystineOrganoselenium CompoundsOxidative StressReactive Oxygen SpeciesApoptosisCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationFerroptosisHCT116 CellsHumansCystineOrganoselenium CompoundsReactive Oxygen Speciesselenocystineapoptosiscolon cancerferroptosisoxidative stressreactive oxygen speciesselenocystine

Identifiers

PMID41887693
PMCPMC13021336

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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.