Evidence map›Paper›PMID 35125808›Full record

ArticleChinese journal of cancer research = Chung-kuo yen cheng yen chiu2021

ZNF292 suppresses proliferation of ESCC cells through ZNF292/SKP2/P27 signaling axis.

Wei Gong, Jiancheng Xu, Guangchao Wang, Dan Li, Qimin Zhan

Open access · diamondAbstract read
In one paragraph

Article in Chinese journal of cancer research = Chung-kuo yen cheng yen chiu, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

10 citing papers in PubMed, 59 citations in OpenAlex.

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  8. Mettl14-mediated mCell reports · 2023
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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

5 authors at 2 institutions in 1 country.

Wei GongState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
Jiancheng XuState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
Guangchao WangState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
Dan LiState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
Qimin ZhanState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIncreasing evidence has demonstrated that ZNF292 plays a suppressive role in cancer, however, little is known about its function and exact mechanism in esophageal squamous cell carcinoma (ESCC).

methodsBioinformatic analysis and immunohistochemistry (IHC) were performed to analyze the role of ZNF292 in affecting the prognosis of ESCC. Cell proliferation and colony formation ability assays were performed to analyze cell growth after inferring the expression of ZNF292. Flow cytometry was used to analyze changes in the cell cycle upon the depletion of ZNF292. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analysis were used to determine the alteration of cell cycle related RNAs and proteins after knocking down ZNF292. MG-132, cycloheximide (CHX) treatment experiments were performed to analyze the change and half-life time of P27 after knockdown of ZNF292. Chromatin immunoprecipitation (ChIP) and luciferase reporter assays were used to analyze the transcriptional regulation of SKP2 by ZNF292.

resultsWe report that low expression of ZNF292 is associated with poor prognosis, and ZNF292 emerges to be highly expressed in adjacent and normal tissues rather than tumor tissues in ESCC. Knockdown of ZNF292 significantly boosts cell growth and S phase entry in ESCC cells. ZNF292 depletion will decrease the expression and half-life time of P27, while knockdown of SKP2 will result in elevated expression of P27. ZNF292 can bind to the promoter region of SKP2, and knockdown of ZNF292 will boost the expression of SKP2.

conclusionsKnockdown of ZNF292 mediates G1/S cell cycle procession by activating SKP2/P27 signaling in ESCC cells. ZNF292 knockdown promotes SKP2 expression at the transcriptional level, thereby boosting P27 ubiquitin-degradation, and eventually facilitating the S phase entrance.

Indexed as

cell cycleESCCSKP2ZNF292

Identifiers

PMID35125808
PMCPMC8742179
OpenAlexW4206831615

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.