Evidence map›Paper›PMID 38347435›Full record

ArticleBMC cancer2024

Oridonin-induced ferroptosis and apoptosis: a dual approach to suppress the growth of osteosarcoma cells.

Feifan Zhang, Yang Hao, Ning Yang, Man Liu, Yage Luo, Ying Zhang, Jian Zhou, Hongjian Liu, Jitian Li

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
9.6field-weighted citation impact, top 1% 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

16 citing papers in PubMed, 23 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

9 authors at 4 institutions in 1 country.

Feifan Zhang *Hunan University of Chinese Medicine, Changsha, China.
Yang Hao *Henan Luoyang Orthopedic Hospital (Henan Provincial Orthopedic Hospital), Zhengzhou, China.
Ning YangHenan Luoyang Orthopedic Hospital (Henan Provincial Orthopedic Hospital), Zhengzhou, China.
Man LiuHenan Luoyang Orthopedic Hospital (Henan Provincial Orthopedic Hospital), Zhengzhou, China.
Yage LuoHenan Luoyang Orthopedic Hospital (Henan Provincial Orthopedic Hospital), Zhengzhou, China.
Ying ZhangHenan Luoyang Orthopedic Hospital (Henan Provincial Orthopedic Hospital), Zhengzhou, China.
Jian ZhouQingdao Hospital, University of Health and Rehabilitation Sciences (Qingdao Municipal Hospital), Qingdao Municipal Hospital, Qingdao, China.
Hongjian LiuDepartment of Orthopedics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. hongjianmd@126.com.
Jitian LiHunan University of Chinese Medicine, Changsha, China. jitianlee@hotmail.com.
Luoyang Orthopedic-Traumatological Hospital of Henan Province · CNFirst Affiliated Hospital of Henan University · CNFirst Affiliated Hospital of Zhengzhou University · CNQingdao Municipal Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteosarcoma (OS) is one of the most common aggressive bone malignancy tumors in adolescents. With the application of new chemotherapy regimens, finding new and effective anti-OS drugs to coordinate program implementation is urgent for the patients of OS. Oridonin had been proved to mediate anti-tumor effect on OS cells, but its mechanism has not been fully elucidated.

methodsThe effects of oridonin on the viability, clonal formation and migration of 143B and U2OS cells were detected by CCK-8, colony formation assays and wound-healing test. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was used to explore the mechanism of oridonin on OS. Western blot (WB), real-time quantitative PCR (qRT-PCR) were used to detect the expression levels of apoptosis and ferroptosis-relative proteins and genes. Annexin V-FITC apoptosis detection kit and flow cytometry examination were used to detect the level of apoptosis. Iron assay kit was used to evaluate the relative Fe

resultsOridonin could effectively inhibit the survival, clonal formation and metastasis of OS cells. The KEGG results indicated that oridonin is associated with the malignant phenotypic signaling pathways of proliferation, migration, and drug resistance in OS. Oridonin was capable of inhibiting expressions of BAX, cl-caspase3, SLC7A11, GPX4 and FTH1 proteins and mRNA, while promoting the expressions of Bcl-2 and ACSL4 in 143B and U2OS cells. Additionally, we found that oridonin could promote the accumulation of reactive oxygen species (ROS) and Fe

conclusionOridonin can trigger apoptosis and ferroptosis collaboratively in OS cells, making it a promising and effective agent for OS therapy.

Indexed as

Diterpenes, KauraneFerroptosisOsteosarcomaAdolescentApoptosisCell Line, TumorCell ProliferationHumansReactive Oxygen SpeciesDiterpenes, KauraneoridoninReactive Oxygen SpeciesAnti-tumorApoptosisFerroptosisOridoninOsteosarcomaROS

Identifiers

PMID38347435
PMCPMC10863210
OpenAlexW4391755808

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Registered trials

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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.