Evidence map›Paper›PMID 35933405›Full record

ArticleCell death & disease2022

shRNA‑mediated knockdown of KNTC1 inhibits non-small-cell lung cancer through regulating PSMB8.

Ruijun Liu, Ruili Liu, Zhiyi Guo, Jianghao Ren, Jia Huang, Qingquan Luo, Qiang Tan

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  3. Biomolecules & biomedicine · 2025
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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 2 institutions in 1 country.

Ruijun LiuShanghai Lung Tumor Clinical Medicine Center, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, 200030, P. R. China.
Ruili LiuDepartment of Stomatology, Ordos central hospital, Ordos, Inner Mongolia, 017000, P. R. China.
Zhiyi GuoShanghai Lung Tumor Clinical Medicine Center, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, 200030, P. R. China.
Jianghao RenShanghai Lung Tumor Clinical Medicine Center, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, 200030, P. R. China.
Jia HuangShanghai Lung Tumor Clinical Medicine Center, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, 200030, P. R. China.
Qingquan LuoShanghai Lung Tumor Clinical Medicine Center, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, 200030, P. R. China. luoqingquan@hotmail.com.
Qiang TanShanghai Lung Tumor Clinical Medicine Center, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, 200030, P. R. China. dr_tanqiang@sina.cn.
Shanghai Jiao Tong University · CNShanghai Chest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In view of the important roles played by Kinetochore proteins in mitosis, we believed that they may contribute to the development and progression of human cancers, which has been reported recently elsewhere. Kinetochore-associated 1 (KNTC1) participates in the segregation of sister chromatids during mitosis, the effects of which on non-small-cell lung cancer (NSCLC) remain unclear. Here, we sought to identify the biological significance of KNTC1 in NSCLC. KNTC1 protein expression in NSCLC tissues was investigated by immunohistochemistry. Lentivirus delivered short hairpin RNA (shRNA) was utilized to establish KNTC1 silence NSCLC cell lines. The effects of KNTC1 depletion on NSCLC cell proliferation, migration, apoptosis, and tumor formation were analyzed by MTT assay, wound-healing assay, transwell assay, flow cytometry assay, and in nude mouse models in vivo. After KNTC1 reduction, NSCLC cell viability, proliferation, migration, and invasion were restrained. A xenograft tumor model was also provided to demonstrate the inhibited tumorigenesis in NSCLC. In addition, the downstream mechanism analysis indicated that KNTC1 depletion was positively associated with PSMB8. The findings of the present study suggested that KNTC1 may have a pivotal role in mediating NSCLC progression and may act as a novel therapeutic target for NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsMicroRNAsRNA, Long NoncodingAnimalsCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMicrotubule-Associated ProteinsProteasome Endopeptidase ComplexRNA, Small InterferingCell Cycle ProteinsKNTC1 protein, humanLMP7 proteinMicroRNAsMicrotubule-Associated ProteinsProteasome Endopeptidase ComplexRNA, Long NoncodingRNA, Small Interfering

Identifiers

PMID35933405
PMCPMC9357013
OpenAlexW4289977724

What OpenQuestion holds

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LicenceCC BY
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.