Evidence map›Paper›PMID 36307402›Full record

ArticleCell death discovery2022

The interplay of transcriptional coregulator NUPR1 with SREBP1 promotes hepatocellular carcinoma progression via upregulation of lipogenesis.

Yongjia Wang, Yuqin Zhang, Zixuan Wang, Lu Yu, Keli Chen, Yuwen Xie, Yang Liu, Weijie Liang, Yilin Zheng, Yizhi Zhan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 27% 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, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  5. Effects of nTiOToxics · 2026
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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

11 authors at 2 institutions in 1 country.

Yongjia Wang *Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong province, China.
Yuqin Zhang *Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong province, China.
Zixuan Wang *The First School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong province, China.
Lu YuDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong province, China.ORCID http://orcid.org/0000-0003-4073-3842
Keli ChenHuiqiao Medical Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong province, China.
Yuwen XieDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong province, China.
Yang LiuDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong province, China.
Weijie LiangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong province, China.
Yilin ZhengDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong province, China.
Yizhi ZhanDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong province, China. yizhi2012@smu.edu.cn.ORCID http://orcid.org/0000-0002-5079-6129
Yi DingDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong province, China. dingyi197980@126.com.ORCID http://orcid.org/0000-0001-5035-9255
Nanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear protein 1 (NUPR1) is a transcriptional coregulator that has been implicated in the development of various cancer types. In addition, de novo fatty acid synthesis plays a pivotal role in hepatocellular carcinoma (HCC) development. However, little is currently known on the role of NUPR1 in hepatocellular carcinoma. In this study, bioinformatics analysis was conducted to analyze the expression level, prognosis value and enriched pathways of NUPR1 in Liver Hepatocellular Carcinoma (LIHC). We found that NUPR1 was significantly upregulated in human hepatocellular carcinoma cells compared with normal hepatocytes from LIHC patients in TCGA cohorts and our patients. Kaplan-Meier analysis and COX proportional hazard progression model showed that high expression of NUPR1 was correlated with a poor prognosis of LIHC patients. CCK-8, EdU and colony formation assays were performed to explore the effect of NUPR1 on the proliferation of HCC cells, then wound healing and transwell migration assays were performed to evaluate the effects of NUPR1 on cell migration. Furthermore, subcutaneous xenograft models were established to study tumor growth. Results showed that NUPR1 overexpression correlated with a highly proliferative and aggressive phenotype. In addition, NUPR1 knockdown significantly inhibited hepatocellular carcinoma cell proliferation and migration in vitro and hindered tumorigenesis in vivo. Mechanistically, endogenous NUPR1 could interact with sterol regulatory element binding protein 1 (SREBP1) and upregulated lipogenic gene expression of fatty acid synthase (FASN), resulting in the accumulation of lipid content. Moreover, pharmacological or genetic blockade of the NUPR1-SREBP1/FASN pathway enhanced anticancer activity in vitro and in vivo. Overall, we identified a novel function of NUPR1 in regulating hepatocellular carcinoma progression via modulation of SREBP1-mediated de novo lipogenesis. Targeting NUPR1-SREBP1/FASN pathway may be a therapeutic alternative for hepatocellular carcinoma.

Identifiers

PMID36307402
PMCPMC9616853
OpenAlexW4307720835

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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.