Evidence map›Paper›PMID 33608495›Full record

ArticleCell death & disease2021

LncRNA CDKN2B-AS1 stabilized by IGF2BP3 drives the malignancy of renal clear cell carcinoma through epigenetically activating NUF2 transcription.

Xina Xie, Jiatian Lin, Xiaoqin Fan, Yuantang Zhong, Yequn Chen, Kaiqing Liu, Yonggang Ren, Xiangling Chen, Daihuan Lai, Xuyi Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  18. Targeting IGF2BP3 in Cancer.International journal of molecular sciences · 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

12 authors at 4 institutions in 1 country.

Xina Xie *Guangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, 518000, Shenzhen, Guangdong, China.
Jiatian Lin *Department of Minimally Invasive Intervention, Peking University Shenzhen Hospital, 518000, Shenzhen, Guangdong, China.
Xiaoqin Fan *Department of Otolaryngology, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, 518000, Shenzhen, Guangdong, China.
Yuantang ZhongDepartment of Urology, Longgang District Central Hospital, 518100, Shenzhen, Guangdong, China.
Yequn ChenDepartment of Community Surveillance, The First Affiliated Hospital of Shantou University Medical College, 515041, Shantou, Guangdong, China.
Kaiqing LiuGuangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, 518000, Shenzhen, Guangdong, China.
Yonggang RenGuangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, 518000, Shenzhen, Guangdong, China.
Xiangling ChenGuangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, 518000, Shenzhen, Guangdong, China.
Daihuan LaiGuangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, 518000, Shenzhen, Guangdong, China.
Xuyi LiGuangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, 518000, Shenzhen, Guangdong, China.
Zesong LiGuangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, 518000, Shenzhen, Guangdong, China. lzssc@yahoo.com.
Aifa TangGuangdong Key Laboratory of Systems Biology and Synthetic Biology for Urogenital Tumors, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, 518000, Shenzhen, Guangdong, China. tangaifa2018@email.szu.edu.cn.ORCID 0000-0002-7516-0506
Shenzhen Second People's Hospital · CNLonggang Central Hospital · CNPeking University Shenzhen Hospital · CNShantou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Because of the lack of sensitivity to radiotherapy and chemotherapy, therapeutic options for renal clear cell carcinoma (KIRC) are scarce. Long noncoding RNAs (lncRNAs) play crucial roles in the progression of cancer. However, their functional roles and upstream mechanisms in KIRC remain largely unknown. Exploring the functions of potential essential lncRNAs may lead to the discovery of novel targets for the diagnosis and treatment of KIRC. Here, according to the integrated analysis of RNA sequencing and survival data in TCGA-KIRC datasets, cyclin-dependent kinase inhibitor 2B antisense lncRNA (CDKN2B-AS1) was discovered to be the most upregulated among the 14 lncRNAs that were significantly overexpressed in KIRC and related to shorter survival. Functionally, CDKN2B-AS1 depletion suppressed cell proliferation, migration, and invasion both in vitro and in vivo. Mechanistically, CDKN2B-AS1 exerted its oncogenic activity by recruiting the CREB-binding protein and SET and MYND domain-containing 3 epigenetic-modifying complex to the promoter region of Ndc80 kinetochore complex component (NUF2), where it epigenetically activated NUF2 transcription by augmenting local H3K27ac and H3K4me3 modifications. Moreover, we also showed that CDKN2B-AS1 interacted with and was stabilized by insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), an oncofetal protein showing increased levels in KIRC. The Kaplan-Meier method and receiver operating curve analysis revealed that patients whose IGF2BP3, CDKN2B-AS1 and NUF2 are all elevated showed the shortest survival time, and the combined panel (containing IGF2BP3, CDKN2B-AS1, and NUF2) possessed the highest accuracy in discriminating high-risk from low-risk KIRC patients. Thus, we conclude that the stabilization of CDKN2B-AS1 by IGF2BP3 drives the malignancy of KIRC through epigenetically activating NUF2 transcription and that the IGF2BP3/CDKN2B-AS1/NUF2 axis may be an ideal prognostic and diagnostic biomarker and therapeutic target for KIRC.

Indexed as

Epigenesis, GeneticRNA StabilityTranscriptional ActivationAnimalsCarcinoma, Renal CellCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationDatabases, GeneticDisease ProgressionDNA MethylationGene Expression Regulation, NeoplasticHumansKidney NeoplasmsMaleCDKN2B antisense RNA, humanCell Cycle ProteinsIGF2BP3 protein, humanNUF2 protein, humanRNA-Binding ProteinsRNA, Long Noncoding

Identifiers

PMID33608495
PMCPMC7895987
OpenAlexW3129331222

What Socratic holds

Textmetadata
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 Socratic graph.