Evidence map›Paper›PMID 35351053›Full record

ArticleBMC cancer2022

NAP1L1 promotes tumor proliferation through HDGF/C-JUN signaling in ovarian cancer.

Xiaohua Zhu, YingYing Xie, Wenyan Huang, Zigui Chen, SuiQun Guo

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.5field-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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

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  16. A New Role of NAP1L1 in Megakaryocytes and Human Platelets.International journal of molecular sciences · 2022
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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

5 authors at 3 institutions in 1 country.

Xiaohua ZhuDepartment of Obstetrics and Gynecology, The Third Affliated Hospital, Southern Medical University, Guangzhou, 510500, Guangdong, China.
YingYing XieCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510315, Guangdong, China.
Wenyan HuangFirst People's Hospital of Zhaoqing, Zhaoqing, 2102013, Guangdong, China.
Zigui ChenCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510315, Guangdong, China.
SuiQun GuoDepartment of Obstetrics and Gynecology, The Third Affliated Hospital, Southern Medical University, 183 Zhongshan Dadaoxi West, Guangzhou, 510500, Guangdong, China. guosq2005@126.Com.
TCM-Intigrated Cancer Center of Southern Medical University · CNThird Affiliated Hospital of Southern Medical University · CNThe First People's Hospital of Zhaoqing · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNucleosome assembly protein 1-like 1 (NAP1L1) is highly expressed in various types of cancer and plays an important role in carcinogenesis, but its specific role in tumor development and progression remains largely unknown. In this study, we suggest the potential of NAP1L1 as a prognostic biomarker and therapeutic target for the treatment of ovarian cancer (OC).

methodsIn our study, a tissue microarray (TMA) slide containing specimens from 149 patients with OC and 11 normal ovarian tissues underwent immunohistochemistry (IHC) to analyze the correlation between NAP1L1 expression and clinicopathological features. Loss-of- function experiments were performed by transfecting siRNA and following lentiviral gene transduction into SKOV3 and OVCAR3 cells. Cell proliferation and the cell cycle were assessed by the Cell Counting Kit-8, EDU assay, flow cytometry, colony formation assay, and Western blot analysis. In addition, co-immunoprecipitation (Co-IP) and immunofluorescence assays were performed to confirm the relationship between NAP1L1 and its potential targets in SKOV3/OVCAR3 cells.

resultsHigh expression of NAP1L1 was closely related to poor clinical outcomes in OC patients. After knocking down NAP1L1 by siRNA or shRNA, both SKOV3 and OVCAR3 cells showed inhibition of cell proliferation, blocking of the G1/S phase, and increased apoptosis in vitro. Mechanism analysis indicated that NAP1L1 interacted with hepatoma-derived growth factor (HDGF) and they were co-localized in the cytoplasm. Furthermore, HDGF can interact with jun proto-oncogene (C-JUN), an oncogenic transformation factor that induces the expression of cyclin D1 (CCND1). Overexpressed HDGF in NAP1L1 knockdown OC cells not only increased the expression of C-JUN and CCND1, but it also reversed the suppressive effects of si-NAP1L1 on cell proliferation.

conclusionsOur data demonstrated that NAP1L1 could act as a prognostic biomarker in OC and can interact with HDGF to mediate the proliferation of OC, and this process of triggered proliferation may contribute to the activation of HDGF/C-JUN signaling in OC cells.

Indexed as

ApoptosisNucleosome Assembly Protein 1Ovarian NeoplasmsCell Line, TumorCell ProliferationFemaleGenes, junHumansIntercellular Signaling Peptides and Proteinshepatoma-derived growth factorIntercellular Signaling Peptides and ProteinsNAP1L1 protein, humanNucleosome Assembly Protein 1CCND1C-JUNHDGFNAP1L1Ovarian cancerProliferation

Identifiers

PMID35351053
PMCPMC8962469
OpenAlexW4220975503

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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.