Evidence map›Paper›PMID 28597490›Full record

ArticleCell proliferation2017

Downregulation of USP32 inhibits cell proliferation, migration and invasion in human small cell lung cancer.

Wenyu Hu, Haiyan Wei, Keming Li, Pei Li, Jiamao Lin, Rui Feng

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2017. 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
1.2field-weighted citation impact, top 21% 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, 35 citations in OpenAlex.

  1. Deubiquitination of Vangl by USP6 and USP32 Regulates Planar Cell Polarity Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

6 authors at 2 institutions in 1 country.

Wenyu HuDepartment of Medicine, Shandong Cancer Hospital and Institute, Ji Nan, Shan Dong, China.
Haiyan WeiPhysical and Chemical Laboratory, Shandong Academy of Occupational Health and Occupational Medicine, Ji Nan, Shandong, China.
Keming LiDepartment of Medicine science, Shandong Academy of Traditional Medicine, Ji Nan, Shandong, China.
Pei LiDepartment of Medicine, Shandong Cancer Hospital and Institute, Ji Nan, Shan Dong, China.
Jiamao LinDepartment of Medicine, Shandong Cancer Hospital and Institute, Ji Nan, Shan Dong, China.
Rui FengDepartment of Medicine, Shandong Cancer Hospital and Institute, Ji Nan, Shan Dong, China.ORCID http://orcid.org/0000-0002-4523-9344
Shandong Tumor Hospital · CNShandong Academy of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesUbiquitin specific protease 32 (USP32) is a highly conserved but uncharacterized gene, which has been reported to be associated with growth of breast cancer cells. However, the role of USP32 in human small cell lung cancer (SCLC) has not been uncovered. The aim of this study was to investigate and evaluate the clinical significance of USP32 in patients with SCLC. MATERIALS AND

methodsExpression of USP32 was firstly investigated using public online data sets and then determined in SCLC tissues and cell lines using quantitative real-time PCR, Western blotting and immunohistochemical staining. SCLC cells were transfected with a small-interfering RNA targeting USP32 mRNA and analysed for cell viability, proliferation ability, cell cycle distribution, apoptosis and invasion.

resultsUSP32 was found to be overexpressed in SCLC tissues compared with normal tissues. High USP32 expression was significantly correlated with disease stage and invasion. In vitro experiments demonstrated that silencing of USP32 caused a significant decrease in the proliferation and migration rate of cells. Furthermore, USP32 silencing arrested cell cycle progression at G0/G1 phase via decreasing CDK4/Cyclin D1 complex and elevating p21. In addition, downregulation of USP32 significantly induced cell apoptosis by activating cleaved caspase-3 and cleaved PARP, as well as inhibiting cell invasiveness via altering epithelial mesenchymal transition expression.

conclusionsOur results suggest for the first time that USP32 is important for SCLC progression and might be a potential target for molecular therapy of SCLC.

Indexed as

AgedCaspase 3Cell MovementCell ProliferationCyclin D1Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p21Down-RegulationFemaleG1 Phase Cell Cycle CheckpointsHumansImmunohistochemistryLung NeoplasmsMalePoly(ADP-ribose) PolymerasesRNA InterferenceCaspase 3Cyclin D1Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p21Poly(ADP-ribose) PolymerasesRNA, MessengerRNA, Small InterferingUbiquitin ThiolesteraseUSP10 protein, humancell apoptosiscell cyclecell proliferationinvasionsmall cell lung cancerUSP32

Identifiers

PMID28597490
PMCPMC6529138
OpenAlexW2622032701

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.