Evidence map›Paper›PMID 31527303›Full record

ArticleAging2019

HnRNPR-CCNB1/CENPF axis contributes to gastric cancer proliferation and metastasis.

Er-Bao Chen, Xuan Qin, Ke Peng, Qian Li, Cheng Tang, Yi-Chou Wei, Shan Yu, Lu Gan, Tian-Shu Liu

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

79 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Proteomic profiling identifies an oncogene ITGA2 and its downstream targets in gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  6. Oncology research · 2026
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19 more citing papers are in PubMed but not listed here.

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

9 authors at 4 institutions in 1 country.

Er-Bao ChenDepartment of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xuan QinSchool of Chemical Biology and Biotechnology, Shenzhen Graduate School of Peking University, Shenzhen, China.
Ke PengDepartment of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China.
Qian LiDepartment of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China.
Cheng TangDepartment of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China.
Yi-Chou WeiDepartment of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China.
Shan YuDepartment of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China.
Lu GanDepartment of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China.
Tian-Shu LiuDepartment of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China.
Fudan University · CNSun Yat-sen University · CNZhongshan Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is a common disease globally with high mortality rate. It is therefore necessary to develop novel therapies targeting specific events in the pathogenesis of GC. Some hnRNP family members are involved in multiple cancer biological behaviors. However, the potential function and mechanism of hnRNPR, a new molecule of hnRNP family in GC remains unknown. We found that the expression of hnRNPR was significantly overexpressed in multiple cancers compared to the normal tissues. Functionally, hnRNPR promoted cancer cell proliferation, migration, and invasion. Knockdown of hnRNPR in two type mice models, with two types of tumors models decreased the tumor aggressiveness and metastasis. Mechanistically, hnRNPR targeted oncogenic pathways by stabilizing the expression of CCNB1 and CENPF mRNA level. Knockdown of CCNB1 and CENPF abolished the hnRNPR-induced cell growth and invasion, respectively. Furthermore, the protein level of hnRNPR in the tumor was positively correlated with the expression of CCNB1 and CENPF in clinical samples. Together, these results indicate that overexpression of hnRNPR promoted the aggressiveness of GC by increasing the mRNA expression of CCNB1 and CENPF. HnRNPR-CCNB1/CENPF axis may be a potential therapeutic target for GC treatment.

Indexed as

AnimalsCell Line, TumorCell ProliferationCell SurvivalChromosomal Proteins, Non-HistoneCyclin B1Gastric MucosaGene Expression Regulation, NeoplasticHeterogeneous-Nuclear RibonucleoproteinsMaleMice, NudeMicrofilament ProteinsNeoplasm MetastasisNeoplasms, ExperimentalRNA InterferenceRNA, MessengerCCNB1 protein, humancentromere protein FChromosomal Proteins, Non-HistoneCyclin B1Heterogeneous-Nuclear RibonucleoproteinsHNRNPR protein, humanMicrofilament ProteinsRNA, MessengerCCNB1CENPFgastric cancerhnRNPRRNA binding protein

Identifiers

PMID31527303
PMCPMC6782008
OpenAlexW2974047793

What OpenQuestion holds

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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.