Evidence map›Paper›PMID 32100243›Full record

ArticleJournal of physiology and biochemistry2020

miR-485-5p/HSP90 axis blocks Akt1 phosphorylation to suppress osteosarcoma cell proliferation and migration via PI3K/AKT pathway.

Qing Liu, Zhenting Wang, Xiaohua Zhou, Mingying Tang, Wei Tan, Tianshi Sun, Yifang Wang, Youwen Deng

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of physiology and biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 59 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

8 authors at 3 institutions in 1 country.

Qing LiuDepartment of Spine Surgery, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Changsha, Hunan, People's Republic of China.
Zhenting WangDepartment of Spine Surgery, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Changsha, Hunan, People's Republic of China.
Xiaohua ZhouDepartment of Spine Surgery, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.
Mingying TangDepartment of Spine Surgery, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.
Wei TanDepartment of Spine Surgery, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Changsha, Hunan, People's Republic of China.
Tianshi SunDepartment of Spine Surgery, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.
Yifang WangDepartment of Spine Surgery, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.
Youwen DengDepartment of Spine Surgery, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Changsha, Hunan, People's Republic of China. drywdeng@csu.edu.cn.
Central South University · CNSecond Xiangya Hospital of Central South University · CNThird Xiangya Hospital · CN

Funding

Hunan Science and Technology Innovation Plan 2018SK2105Hunan Science and Technology Innovation Plan kq1606001the Fundamental Research Funds for the Central Universities 2019zzts019the Fundamental Research Funds for the Central Universities 2019zzts809the Key Scientific Research and Innovation Projects of Hunan Postgraduates CX20190074
6 · The paper itself

Abstract

Osteosarcoma (OS) is closely related to the dysregulation of various intracellular signaling pathways, especially the PI3K/Akt signaling pathway. Reportedly, HSP90 was responsible for phospho-Akt stabilization, and both AKT1 and HSP90 were upregulated within osteosarcoma. Herein, we demonstrated that AKT1 and HSP90 mRNA and protein expression were upregulated within osteosarcoma tissues and cells; AKT1 knockdown significantly inhibited OS cell viability. HSP90 knockdown suppressed the phosphorylation of AKT1, decreased ki-67 and Vimentin protein levels, enhanced p21 and E-cadherin protein levels, and inhibited OS cell proliferation and migration; AKT1 overexpression exerted opposing effects and significantly attenuated the effects of HSP90 knockdown. miR-485-5p targeted AKT1 and HSP90 3'-UTR to inhibit AKT1 and HSP90 expression. miR-485-5p overexpression dramatically reduced AKT1, HSP90, and ki-67 proteins, increased E-cadherin protein levels, and inhibited OS cell proliferation and migration. In conclusion, HSP90 knockdown blocked the phosphorylation of AKT1 suppressing the proliferation and migration capacity of OS cells via the PI3K/AKT pathway; miR-485-5p binds to HSP90 and AKT1 in their 3'-UTR to inhibit HSP90 and AKT1 expression, therefore exerting a tumor suppressor function within osteosarcoma.

Indexed as

Signal TransductionBone NeoplasmsCell Line, TumorCell MovementCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansMicroRNAsOsteosarcomaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAKT1 protein, humanHSP90 Heat-Shock ProteinsMicroRNAsMIRN485 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAKT1HSP90miR-485-5pOsteosarcoma (OS)PI3K/AKT signaling pathway

Identifiers

PMID32100243
OpenAlexW3008006076

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.