Evidence map›Paper›PMID 33622397›Full record

ArticleCell & bioscience2021

DNA primase subunit 1 deteriorated progression of hepatocellular carcinoma by activating AKT/mTOR signaling and UBE2C-mediated P53 ubiquitination.

Mengqi Zhu, Mengna Wu, Saiyan Bian, Qianqian Song, Mingbing Xiao, Hua Huang, Li You, Jianping Zhang, Jie Zhang, Chun Cheng and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
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  8. Proteo-genomic characterization of cirrhosis-associated liver cancers reveals potential subtypes and therapeutic targets.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  9. Article
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  12. Role of UBE2C in Brain Cancer Invasion and Dissemination.International journal of molecular sciences · 2023
    Review
  13. Combined Inhibition ofInternational journal of molecular sciences · 2023
    Article
  14. Identification of acetyl-CoA carboxylase alpha as a prognostic and targeted candidate for hepatocellular carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 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 2 institutions in 2 countries.

Mengqi Zhu *Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China.
Mengna Wu *Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China.
Saiyan Bian *Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China.
Qianqian SongDepartment of Radiology, Wake Forest School of Medicine, One Medical Center Boulevard, Winston-Salem, 27157 NC, USA.
Mingbing XiaoResearch Center of Clinical Medicine, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China.
Hua HuangResearch Center of Clinical Medicine, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China.
Li YouResearch Center of Clinical Medicine, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China.
Jianping ZhangResearch Center of Clinical Medicine, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China.
Jie ZhangDepartment of Oncology, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China.
Chun ChengSchool of Medicine, Nantong University, 19 Qixiu Road, Nantong, 226001, Jiangsu, China.
Wenkai NiResearch Center of Clinical Medicine, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China. niwenkai@sina.com.
Wenjie ZhengResearch Center of Clinical Medicine, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong, 226001, Jiangsu, China. zwj007008009@163.com.ORCID http://orcid.org/0000-0002-3073-4596
Nantong University · CNWake Forest University · US

Funding

Jiangsu Provincial Key Research and Development Program BE2020668Nantong Science and Technology Bureau MS12019013Nantong Science and Technology Bureau MS12020020National Natural Science Foundation of China 81702419National Natural Science Foundation of China 82070622
6 · The paper itself

Abstract

backgroundDNA primase subunit 1 (PRIM1) has been reported as a novel oncogene in several cancer types. However, its roles in hepatocellular carcinoma (HCC) remain unclear. This study aimed to investigate underlying mechanisms of PRIM1 and identify it as a potential molecular target for HCC.

methodsHub genes were screened between HCC tissues and normal liver tissues in 3 gene expression omnibus (GEO) datasets and the cancer genome atlas (TCGA). The expression features and prognostic value of one of the hub genes PRIM1 were analyzed by bioinformatic analyses and immunohistochemistry. Loss-of-function and gain-of-function studies were used to investigate the regulatory role of PRIM1 in HCC cells. Real-time (RT)-qPCR, western blotting, and ubiquitin immunoprecipitation assays were performed to explore the underlying mechanisms. The xenograft model was employed to detect the roles of PRIM1 in tumor growth in vivo. Finally, the 3D spheroid model was conducted to validate the role of PRIM1 in tumor growth and sorafenib resistance.

resultsThe hub genes of HCC were screened in multiple bioinformatic datasets. PRIM1, as one of the hub genes, was significantly overexpressed in HCC tissues in mRNA and protein levels. In addition, high expression of PRIM1 indicated poor prognosis of HCC patients in TCGA, ICGC, and Nantong cohorts. Overexpression of PRIM1 promoted the proliferation, migration/invasion, and sorafenib resistance of HCC cells, with the decrease in apoptosis and cell cycle arrest. Mechanically, PRIM1 facilitated epithelial-mesenchymal transition (EMT) process and the activity of PI3K/AKT/mTOR signaling of HCC cells. Additionally, PRIM1 could cause the ubiquitination and degradation of P53 by upregulating Ubiquitin Conjugating Enzyme E2 C (UBE2C). Furthermore, knockdown of PRIM1 significantly inhibited the growth of xenograft tumors and HCC cells-derived spheroids with enhanced sorafenib resistance.

conclusionThis study implies that PRIM1 may play a key role in the progression of HCC and may serve as a potential target for HCC treatment.

Indexed as

AKT/mTORDNA primase subunit 1Hepatocellular carcinomaMolecular targetP53

Identifiers

PMID33622397
PMCPMC7903777
OpenAlexW3129600143

What OpenQuestion holds

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LicenceCC BY
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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.