Evidence map›Paper›PMID 30931932›Full record

ArticleCell death & disease2019

Anoikis resistant mediated by FASN promoted growth and metastasis of osteosarcoma.

Tianhao Sun, Xing Zhong, Honghai Song, Jiaming Liu, Jingao Li, Frankie Leung, William W Lu, Zhi-Li Liu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

38 citing papers in PubMed, 77 citations in OpenAlex.

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  18. Metabolic reprogramming in osteosarcoma.Pediatric discovery · 2023
    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

8 authors at 4 institutions in 2 countries.

Tianhao SunDepartment of Orthopedic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Xing ZhongDepartment of Orthopedic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Honghai SongDepartment of Orthopedic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Jiaming LiuDepartment of Orthopedic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Jingao LiDivision of Chemotherapy, Jiangxi Cancer Hospital, Nanchang, Jiangxi Province, China.
Frankie LeungDepartment of Orthopaedics and Traumatology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. klleunga@hku.hk.
William W LuDepartment of Orthopaedics and Traumatology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. wwlu@hku.hk.
Zhi-Li LiuDepartment of Orthopedic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China. zgm7977@163.com.
University of Hong Kong · HKFirst Affiliated Hospital of Nanchang University · CNJiangxi Provincial Cancer Hospital · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pulmonary metastasis of osteosarcoma (OS) occurs commonly, which resulted from anoikis resistant (AR) of tumor cells as reported by previous studies, but the exact roles of AR in osteosarcoma were not fully studied. Our previous investigations showed fatty acid synthase (FASN) was relating to clinical features of patients with OS. In this study, we aim to explore the functions of FASN in the AR OS cells in vitro and in vivo and study the downstream effectors of FASN. In the present study, we used our established cell model to study the AR. We revealed that AR promoted cell proliferation and migration as determined by colony formation assay and transwell assay. In addition, AR assisted tumor growth in vivo. In the AR cells, the expression of FASN was higher. Thus, we constructed lentiviruses to silence or overexpress FASN in four cell lines to study functions of FASN. Silence of FASN reduced cell colonies and migration while overexpression of FASN increased colonies and migration in suspended cells. Loss of functions of FASN induced cell apoptosis in suspended OS cells while gain of function of FASN suppressed apoptosis as determined by flow cytometry. We found the levels of p-ERK1/2 and Bcl-xL declined when FASN was silenced while they increased when FASN was overexpressed. In addition, results showed that the levels of FASN and its potential related molecules (p-ERK1/2 and Bcl-xL) increased in 143B-AR and MG-63-AR cells. In vivo study showed that inhibition of FASN decreased pulmonary metastasis of OS. In conclusion, we showed that anoikis resistant and FASN as two interactional factors facilitated the progress of osteosarcoma.

Indexed as

AnoikisAnimalsApoptosisbcl-X ProteinBone NeoplasmsCell Line, TumorCell MovementCell ProliferationFatty Acid Synthase, Type IFemaleGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudeMitogen-Activated Protein Kinase 3bcl-X ProteinFASN protein, humanFatty Acid Synthase, Type IMAPK3 protein, humanMitogen-Activated Protein Kinase 3

Identifiers

PMID30931932
PMCPMC6443797
OpenAlexW2932064109

What OpenQuestion holds

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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.