Evidence map›Paper›PMID 33173727›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2020

A p53/lnc-Ip53 Negative Feedback Loop Regulates Tumor Growth and Chemoresistance.

Li-Zhen Zhang, Jin-E Yang, Yu-Wei Luo, Feng-Ting Liu, Yun-Fei Yuan, Shi-Mei Zhuang

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

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  5. CENPF as a prognostic marker of glioma: unraveling the molecular mechanisms.Journal of cancer research and clinical oncology · 2025
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  9. GINS4 suppresses ferroptosis by antagonizing p53 acetylation with Snail.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  10. Heliyon · 2023
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  13. Targeting NK-1R attenuates renal fibrosisFrontiers in immunology · 2023
    Article
  14. Article
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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

6 authors at 1 institution in 1 country.

Li-Zhen ZhangMOE Key Laboratory of Gene Function and Regulation School of Life Sciences Collaborative Innovation Center for Cancer Medicine Sun Yat-sen University Guangzhou 510275 China.
Jin-E YangMOE Key Laboratory of Gene Function and Regulation School of Life Sciences Collaborative Innovation Center for Cancer Medicine Sun Yat-sen University Guangzhou 510275 China.
Yu-Wei LuoMOE Key Laboratory of Gene Function and Regulation School of Life Sciences Collaborative Innovation Center for Cancer Medicine Sun Yat-sen University Guangzhou 510275 China.
Feng-Ting LiuMOE Key Laboratory of Gene Function and Regulation School of Life Sciences Collaborative Innovation Center for Cancer Medicine Sun Yat-sen University Guangzhou 510275 China.
Yun-Fei YuanDepartment of Hepatobilliary Oncology Cancer Center Sun Yat-sen University Guangzhou 510060 China.
Shi-Mei ZhuangMOE Key Laboratory of Gene Function and Regulation School of Life Sciences Collaborative Innovation Center for Cancer Medicine Sun Yat-sen University Guangzhou 510275 China.ORCID https://orcid.org/0000-0002-2512-3942
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetylation is a critical mechanism to modulate tumor-suppressive activity of p53, but the causative roles of long non-coding RNAs (lncRNAs) in p53 acetylation and their biological significance remain unexplored. Here, lncRNA LOC100294145 is discovered to be transactivated by p53 and is thus designated as lnc-Ip53 for lncRNA induced by p53. Furthermore, lnc-Ip53 impedes p53 acetylation by interacting with histone deacetylase 1 (HDAC1) and E1A binding protein p300 (p300) to prevent HDAC1 degradation and attenuate p300 activity, resulting in abrogation of p53 activity and subsequent cell proliferation and apoptosis resistance. Mouse xenograft models reveal that lnc-Ip53 promotes tumor growth and chemoresistance in vivo, which is attenuated by an HDAC inhibitor. Silencing lnc-Ip53 inhibits the growth of xenografts with wild-type p53, but not those expressing acetylation-resistant p53. Consistently, lnc-Ip53 is upregulated in multiple cancer types, including hepatocellular carcinoma (HCC). High levels of lnc-Ip53 is associated with low levels of acetylated p53 in human HCC and mouse xenografts, and is also correlated with poor survival of HCC patients. These findings identify a novel p53/lnc-Ip53 negative feedback loop in cells and indicate that abnormal upregulation of lnc-Ip53 represents an important mechanism to inhibit p53 acetylation/activity and thereby promote tumor growth and chemoresistance, which may be exploited for anticancer therapy.

Indexed as

acetylationlnc‐Ip53non‐coding RNAp53tumor growth

Identifiers

PMID33173727
PMCPMC7610266
OpenAlexW3090619328

What OpenQuestion holds

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Read underepoch 390

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.