Evidence map›Paper›PMID 32926297›Full record

ArticleMolecular and cellular biochemistry2021

Heat shock protein B8 promotes proliferation and migration in lung adenocarcinoma A549 cells by maintaining mitochondrial function.

Ling-Ling Yu, Yuan Wang, Zu-Ke Xiao, Sheng-Song Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 25 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

4 authors at 2 institutions in 1 country.

Ling-Ling YuDepartment of Rehabilitation Medicine, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang, 330006, Jiangxi, People's Republic of China.
Yuan WangDepartment of Graduate School, Gansu University of Chinese Medicine, No. 35 Dingxi East Road, Chengguan District, 730000, Lanzhou, People's Republic of China.
Zu-Ke XiaoDepartment of Pulmonary and Critical Care Medicine, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, No. 92 Aiguo Road, Nanchang, 330006, Jiangxi, People's Republic of China.
Sheng-Song ChenDepartment of Pulmonary and Critical Care Medicine, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, No. 92 Aiguo Road, Nanchang, 330006, Jiangxi, People's Republic of China. chenss93@163.com.ORCID http://orcid.org/0000-0003-2763-943X
Nanchang University · CNGansu University of Traditional Chinese Medicine · CN

Funding

Natural Science Foundation of Jiangxi Province 20202BAB206042the National Natural Science Foundation excellent youth cultivation project 20202ZDB01017the Natural Science Foundation of Jiangxi Province 20202BABL216035the Science and technology plan project of Jiangxi Administration of traditional Chinese Medicine, China 2019A067
6 · The paper itself

Abstract

Heat shock protein B8 (HSPB8) impacts on tumor proliferation and migration of malignancy. However, the role of HSPB8 in lung adenocarcinoma (LUAC) remains unclear. The aim of this study, therefore, was to clarify whether HSPB8 could bring benefits to proliferation and migration of LUAC and its underlying mechanisms. The expression of HSPB8 was first evaluated by immunohistochemistry in 35 LUAC samples. Then, A549 lung adenocarcinoma cells were transfected with pcDNA-HSPB8 or si-HSPB8 to induce HSPB8 overexpression and silence. Cellular activity was evaluated with a Cell Counting Kit-8 (CCK-8) assay. Cell proliferation and migration were observed by EdU assay and scratch assay. Mitochondria-specific reactive oxygen species (mtROS) and membrane potential were measured using MitoSOX Red probe and JC-1 staining. Superoxide dismutase (SOD) activities and malondialdehyde (MDA) level were measured using commercial kits, respectively. HSPB8 protein, mitochondrial fusion protein MFN2 and mitochondrial fission protein p-Drp1/Drp1 were measured using western blot. Compared with the normal tissues, the expression of HSPB8 protein was higher in LUAC tissues and upregulation of HSPB8 protein was related to tumor size and tumor location. Furthermore, HSPB8 overexpression aggravated cell proliferation and migration of A549 cells. Mechanistically, HSPB8 suppressed mitochondrial impairment, leading to promoting the progress of A549 lung adenocarcinoma cells. These data demonstrate that HSPB8 plays an important role in progression of LUAC and may be a new target to treat LUAC.

Indexed as

Cell MovementCell ProliferationA549 CellsAdenocarcinoma of LungAgedCell Line, TumorDisease ProgressionFemaleHeat-Shock ProteinsHumansLung NeoplasmsMaleMiddle AgedMitochondriaMolecular ChaperonesOxidative StressHeat-Shock ProteinsHSPB8 protein, humanMolecular ChaperonesReactive Oxygen SpeciesSuperoxide DismutaseA549 cellsHeat shock protein B8Lung adenocarcinomaMigrationMitochondrial functionProliferation

Identifiers

PMID32926297
OpenAlexW3086606927

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.