Evidence map›Paper›PMID 36147467›Full record

ArticleInternational journal of biological sciences2022

SPC25 promotes proliferation and stemness of hepatocellular carcinoma cells via the DNA-PK/AKT/Notch1 signaling pathway.

Jieying Yang, Yue Huang, Mengjia Song, Qiuzhong Pan, Jingjing Zhao, Junyi He, Dijun Ouyang, Chaopin Yang, Yulong Han, Yan Tang and 7 more

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 39 citations in OpenAlex.

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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

17 authors at 3 institutions in 1 country.

Jieying YangDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Yue HuangDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Mengjia SongDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Qiuzhong PanDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Jingjing ZhaoDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Junyi HeDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Dijun OuyangDepartment of Oncology, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China.
Chaopin YangDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Yulong HanDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Yan TangDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Qijing WangDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Jia HeDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Yongqiang LiDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Hao ChenDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Desheng WengDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Tong XiangDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
JianChuan XiaDepartment of Biotherapy, Sun Yat-sen University Cancer Center, Guangzhou, China.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNFifth Affiliated Hospital of Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The imbalance of kinetochore-microtubule attachment during cell mitosis is a response to the initiation and progression of human cancers. Spindle component 25 (SPC25) is indispensable for spindle apparatus organization and chromosome segregation. SPC25 plays an important role in the development of malignant tumors, but its role in hepatocellular carcinoma (HCC) is yet to be determined. In this study, we aimed to preliminarily investigate the role of SPC25 in HCC progression and the molecular mechanisms underlying the process. We identified SPC25 as a clinically notable molecule significantly correlated with the grade of malignancy and poor survival in both The Cancer Genome Atlas (TCGA) cohort and the HCC patient cohort from our center. Mechanistically, SPC25 promoted the incidence of DNA damage and activated the DNA-PK/Akt/Notch1 signaling cascade in HCC cells; the NICD/ RBP-Jκ complex directly targeted SOX2 and NANOG in a transcriptional manner to regulate the proliferation and self-renewal of HCC cells. Our study suggests that HCC-intrinsic SPC25/DNA-PK/Akt/Notch1 signaling is an important mechanism to promote carcinogenesis by regulating the proliferation and stemness program, which provides possible biomarkers for predicting HCC progression and poor survival, as well as potential therapeutic targets for HCC patients.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsMicrotubule-Associated ProteinsCell Line, TumorCell ProliferationDNAGene Expression Regulation, NeoplasticHumansProto-Oncogene Proteins c-aktReceptor, Notch1Signal TransductionDNAMicrotubule-Associated ProteinsNOTCH1 protein, humanProto-Oncogene Proteins c-aktReceptor, Notch1SPC25 protein, humanDNA-PK/AKThepatocellular carcinomaNotch1SPC25stemness

Identifiers

PMID36147467
PMCPMC9461674
OpenAlexW4293109911

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.