Evidence map›Paper›PMID 34239933›Full record

ArticleBioMed research international2021

The Silence of PSMC6 Inhibits Cell Growth and Metastasis in Lung Adenocarcinoma.

Jian-Yu Zhang, Ke-Zhi Shi, Xiang-Yu Liao, Shi-Jun Li, Dan Bao, Ying Qian, Dao-Jun Li

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 22 citations in OpenAlex.

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  4. Comprehensive analysis reveals the prognostic and immunological role of PSMD13 in hepatocellular carcinoma.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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  16. Frontiers in oncology · 2022
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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

7 authors at 1 institution in 1 country.

Jian-Yu ZhangThe First College of Clinical Medical Science, Three Gorges University & Yichang Central People's Hospital, Yichang, China.
Ke-Zhi ShiThe First College of Clinical Medical Science, Three Gorges University & Yichang Central People's Hospital, Yichang, China.
Xiang-Yu LiaoThe First College of Clinical Medical Science, Three Gorges University & Yichang Central People's Hospital, Yichang, China.
Shi-Jun LiThe First College of Clinical Medical Science, Three Gorges University & Yichang Central People's Hospital, Yichang, China.
Dan BaoThe First College of Clinical Medical Science, Three Gorges University & Yichang Central People's Hospital, Yichang, China.
Ying QianThe First College of Clinical Medical Science, Three Gorges University & Yichang Central People's Hospital, Yichang, China.
Dao-Jun LiThe First College of Clinical Medical Science, Three Gorges University & Yichang Central People's Hospital, Yichang, China.ORCID https://orcid.org/0000-0002-0299-3742
Yichang Central People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The proteasome has been validated as an anticancer drug target, while the role of a subunit of proteasome, PSMC6, in lung adenocarcinoma (LUAD) has not been fully unveiled. In this study, we observed that both the RNA and protein of PSMC6 were highly upregulated in LUAD compared with the adjacent normal tissues. Moreover, a high PSMC6 expression was associated with poor prognosis. In accordance with this finding, PSMC6 was associated with poor tumor differentiation. Furthermore, the silence of PSMC6 by small interference RNAs (siRNAs) could significantly inhibit cell growth, migration, and invasion in lung cancer cell lines, suggesting that PSMC6 might serve as a promising therapeutic target in LUAD. To further explore the molecular mechanism of PSMC6 in LUAD, we observed that the proteasome subunits, such as PSMD10, PSMD6, PSMD9, PSMD13, PSMB3, PSMB1, PSMA4, PSMC1, PSMC2, PSMD7, and PSMD14, were highly correlated with PSMC6 expression. Based on the gene set enrichment analysis, we observed that these proteasome subunits were involved in the degradation of AXIN protein. The correlation analysis revealed that the positively correlated genes with PSMC6 were highly enriched in WNT signaling-related pathways, demonstrating that the PSMC6 overexpression may activate WNT signaling via degrading the AXIN protein, thereby promoting tumor progression. In summary, we systematically evaluated the differential expression levels and prognostic values of PSMC6 and predicted its biological function in LUAD, which suggested that PSMC6 might act as a promising therapeutic target in LUAD.

Indexed as

Gene SilencingA549 CellsAdenocarcinoma of LungATPases Associated with Diverse Cellular ActivitiesCell DifferentiationCell MovementCell ProliferationGene Expression ProfilingGene Expression Regulation, NeoplasticGenome, HumanHumansLung NeoplasmsNeoplasm InvasivenessNeoplasm MetastasisProportional Hazards ModelsProteasome Endopeptidase ComplexATPases Associated with Diverse Cellular ActivitiesProteasome Endopeptidase ComplexPSMC6 protein, humanRNA, Small Interfering

Identifiers

PMID34239933
PMCPMC8235974
OpenAlexW3175783747

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.