Evidence map›Paper›PMID 35597996›Full record

ArticleCancer cell international2022

KMT2B promotes the growth of renal cell carcinoma via upregulation of SNHG12 expression and promotion of CEP55 transcription.

Jia-Fu Feng, Jun Wang, Gang Xie, Yao-Dong Wang, Xiao-Han Li, Wen-Yu Yang, Yu-Wei Yang, Bin Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 8 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

8 authors at 3 institutions in 1 country.

Jia-Fu Feng *NHC Key Laboratory of Nuclear Technology Medical Transformation, Mianyang Central Hospital, School of Medicine, University of Electronic Science and Technology of China, No. 12 Changjia Lane, Jingzhong Street, Mianyang, 621000, People's Republic of China. fengjiafu@uestc.edu.cn.ORCID http://orcid.org/0000-0002-1714-4110
Jun Wang *College of Medical Technology, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, People's Republic of China.
Gang Xie *NHC Key Laboratory of Nuclear Technology Medical Transformation, Mianyang Central Hospital, School of Medicine, University of Electronic Science and Technology of China, No. 12 Changjia Lane, Jingzhong Street, Mianyang, 621000, People's Republic of China.
Yao-Dong WangNHC Key Laboratory of Nuclear Technology Medical Transformation, Mianyang Central Hospital, School of Medicine, University of Electronic Science and Technology of China, No. 12 Changjia Lane, Jingzhong Street, Mianyang, 621000, People's Republic of China.
Xiao-Han LiMedical Laboratory, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, People's Republic of China.
Wen-Yu YangCollege of Medical Technology, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, People's Republic of China.
Yu-Wei YangNHC Key Laboratory of Nuclear Technology Medical Transformation, Mianyang Central Hospital, School of Medicine, University of Electronic Science and Technology of China, No. 12 Changjia Lane, Jingzhong Street, Mianyang, 621000, People's Republic of China.
Bin ZhangNHC Key Laboratory of Nuclear Technology Medical Transformation, Mianyang Central Hospital, School of Medicine, University of Electronic Science and Technology of China, No. 12 Changjia Lane, Jingzhong Street, Mianyang, 621000, People's Republic of China.
University of Electronic Science and Technology of China · CNChengdu University of Traditional Chinese Medicine · CNAffiliated Hospital of Southwest Medical University · CN

Funding

the Science and Technology Department of Sichuan Province 2015SZ0117the Science and Technology Department of Sichuan Province 2019YJ0701the Science and Technology Department of Sichuan Province 2021YJ0239
6 · The paper itself

Abstract

backgroundThis study aims to clarify the mechanistic action of long non-coding RNA (lncRNA) SNHG12 in the development of renal cell carcinoma (RCC), which may be associated with promoter methylation modification by KMT2B and the regulation of the E2F1/CEP55 axis.

methodsTCGA and GEO databases were used to predict the involvement of SNHG12 in RCC. Knockdown of SNHG12/E2F1/CEP55 was performed. Next, SNHG12 expression and other mRNAs were quantified by RT-qPCR. Subsequently, CCK-8 was used to detect cell proliferation. Wound healing assay and Transwell assay were used to detect cell migration and invasion, respectively. The in vitro angiogenesis of human umbilical vein endothelial cells (HUVECs) was explored by matrigel-based capillary-like tube formation assay. ChIP assay was used to detect H3K4me3 in SNHG12 promoter region. The binding of E2F1 to CEP55 promoter region was analyzed with ChIP and dual luciferase reporter assays. RIP assay was used to detect the binding of SNHG12 to E2F1. Finally, the effect of SNHG12 on the tumor formation and angiogenesis of RCC was assessed in nude mouse xenograft model.

resultsSNHG12 was highly expressed in RCC tissues and cells, and it was related to the poor prognosis of RCC patients. SNHG12 knockdown significantly inhibited RCC cell proliferation, migration, and invasion and HUVEC angiogenesis. KMT2B up-regulated SNHG12 expression through modifying H3K4me3 in its promoter region. In addition, SNHG12 promoted CEP55 expression by recruiting the transcription factor E2F1. Knockdown of SNHG12 blocked E2F1 recruitment and down-regulated the expression of CEP55, thereby inhibiting tumor formation and angiogenesis in nude mice.

conclusionThe evidence provided by our study highlighted the involvement of KMT2B in up-regulation of lncRNA as well as the transcription of CEP55, resulting in the promotion of angiogenesis and growth of RCC.

Indexed as

AngiogenesisCEP55E2F1H3K4me3KMT2BLong non-coding RNARenal cell carcinomaSNHG12

Identifiers

PMID35597996
PMCPMC9123657
OpenAlexW4281259467

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.