Evidence map›Paper›PMID 34671012›Full record

ArticleCell death & disease2021

LncRNA SNHG17 interacts with LRPPRC to stabilize c-Myc protein and promote G1/S transition and cell proliferation.

Jin-Yu Liu, Ya-Jing Chen, Huan-Hui Feng, Zhan-Li Chen, Yun-Long Wang, Jin-E Yang, Shi-Mei Zhuang

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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.1field-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

32 citing papers in PubMed, 97 citations in OpenAlex.

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  14. Establishment of a prognostic model based on mJournal of cancer research and clinical oncology · 2023
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  17. Long Non-Coding RNAs as "MYC Facilitators".Pathophysiology : the official journal of the International Society for Pathophysiology · 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

7 authors at 1 institution in 1 country.

Jin-Yu LiuMOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Xin Gang Xi Road 135#, Guangzhou, 510275, P. R. China.ORCID 0000-0001-9179-9302
Ya-Jing ChenMOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Xin Gang Xi Road 135#, Guangzhou, 510275, P. R. China.
Huan-Hui FengMOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Xin Gang Xi Road 135#, Guangzhou, 510275, P. R. China.
Zhan-Li ChenMOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Xin Gang Xi Road 135#, Guangzhou, 510275, P. R. China.
Yun-Long WangMOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Xin Gang Xi Road 135#, Guangzhou, 510275, P. R. China.
Jin-E YangMOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Xin Gang Xi Road 135#, Guangzhou, 510275, P. R. China. lssyje@mail.sysu.edu.cn.ORCID 0000-0002-7511-1042
Shi-Mei ZhuangMOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Xin Gang Xi Road 135#, Guangzhou, 510275, P. R. China. zhuangshimei@163.com.ORCID 0000-0002-2512-3942
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncogenic c-Myc is a master regulator of G1/S transition. Long non-coding RNAs (lncRNAs) emerge as new regulators of various cell activities. Here, we found that lncRNA SnoRNA Host Gene 17 (SNHG17) was elevated at the early G1-phase of cell cycle. Both gain- and loss-of function studies disclosed that SNHG17 increased c-Myc protein level, accelerated G1/S transition and cell proliferation, and consequently promoted tumor cell growth in vitro and in vivo. Mechanistically, the 1-150-nt of SNHG17 physically interacted with the 1035-1369-aa of leucine rich pentatricopeptide repeat containing (LRPPRC) protein, and disrupting this interaction abrogated the promoting role of SNHG17 in c-Myc expression, G1/S transition, and cell proliferation. The effect of SNHG17 in stimulating cell proliferation was attenuated by silencing c-Myc or LRPPRC. Furthermore, silencing SNHG17 or LRPPRC increased the level of ubiquitylated c-Myc and reduced the stability of c-Myc protein. Analysis of human hepatocellular carcinoma (HCC) tissues revealed that SNHG17, LRPPRC, and c-Myc were significantly upregulated in HCC, and they showed a positive correlation with each other. High level of SNHG17 or LRPPRC was associated with worse survival of HCC patients. These data suggest that SNHG17 may inhibit c-Myc ubiquitination and thus enhance c-Myc level and facilitate proliferation by interacting with LRPPRC. Our findings identify a novel SNHG17-LRPPRC-c-Myc regulatory axis and elucidate its roles in G1/S transition and tumor growth, which may provide potential targets for cancer therapy.

Indexed as

AnimalsCell Line, TumorCell ProliferationG1 PhaseGene Expression Regulation, NeoplasticGene SilencingHEK293 CellsHumansMaleMiceModels, BiologicalNeoplasm ProteinsPhosphorylationProtein StabilityProto-Oncogene Proteins c-mycRNA, Long NoncodingLRPPRC protein, humanMYC protein, humanNeoplasm ProteinsProto-Oncogene Proteins c-mycRNA, Long Noncoding

Identifiers

PMID34671012
PMCPMC8528917
OpenAlexW3206279467

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.