Evidence map›Paper›PMID 28849112›Full record

ArticleOncology reports2017

Knockdown of RRS1 by lentiviral-mediated RNAi promotes apoptosis and suppresses proliferation of human hepatocellular carcinoma cells.

Jitao Wang, Zhi Li, Changzeng Zuo, Qingfan Xie, Hui Li, Junhong Jia, Zhongguang Zhen, Ruizhao Qi, Zhiwei Li, Dengxiang Liu and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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  7. Genomic gain ofScience advances · 2021
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  15. Functional role of RRS1 in breast cancer cell proliferation.Journal of cellular and molecular medicine · 2018
    Article
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 3 institutions in 1 country.

Jitao WangDepartment of Hepatobiliary Surgery, The Affiliated Xingtai People's Hospital of Hebei Medical University; Institute of Tumor Disease of Xingtai City, Xingtai, Hebei 054001, P.R. China.
Zhi LiDepartment of Medicine, General Hospital of Jizhong Energy Xingtai Mining Group Limited Liability Company, Xingtai, Hebei 054000, P.R. China.
Changzeng ZuoDepartment of Hepatobiliary Surgery, The Affiliated Xingtai People's Hospital of Hebei Medical University; Institute of Tumor Disease of Xingtai City, Xingtai, Hebei 054001, P.R. China.
Qingfan XieDepartment of Hepatobiliary Surgery, The Affiliated Xingtai People's Hospital of Hebei Medical University; Institute of Tumor Disease of Xingtai City, Xingtai, Hebei 054001, P.R. China.
Hui LiDepartment of Hepatobiliary Surgery, The Affiliated Xingtai People's Hospital of Hebei Medical University; Institute of Tumor Disease of Xingtai City, Xingtai, Hebei 054001, P.R. China.
Junhong JiaDepartment of Hepatobiliary Surgery, The Affiliated Xingtai People's Hospital of Hebei Medical University; Institute of Tumor Disease of Xingtai City, Xingtai, Hebei 054001, P.R. China.
Zhongguang ZhenDepartment of Hepatobiliary Surgery, The Affiliated Xingtai People's Hospital of Hebei Medical University; Institute of Tumor Disease of Xingtai City, Xingtai, Hebei 054001, P.R. China.
Ruizhao QiDepartment of Hepatobiliary Surgery, Beijing 302 Hospital, Beijing 100039, P.R. China.
Zhiwei LiDepartment of Hepatobiliary Surgery, Beijing 302 Hospital, Beijing 100039, P.R. China.
Dengxiang LiuDepartment of Hepatobiliary Surgery, The Affiliated Xingtai People's Hospital of Hebei Medical University; Institute of Tumor Disease of Xingtai City, Xingtai, Hebei 054001, P.R. China.
Baijun SunDepartment of Hepatobiliary Surgery, Beijing 302 Hospital, Beijing 100039, P.R. China.
302 Military Hospital of China · CNXingtai People's Hospital · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years it was found that the synthesis and biological activity of ribosomes are closely associated with tumor cell growth, tumorigenesis, and malignant transformation. However, the role of regulator of ribosome synthesis 1 (RRS1) in hepatocellular carcinoma (HCC) has not yet been reported. In the present study, we aimed to examine the potential role of RRS1 in tumor cell growth by using a lentivirus-mediated RNA interference (RNAi) system in the HCC cell line SMMC-7721 in vitro. Compared with that of the negative control group (Lv-shCon), the mRNA and protein expression levels of RRS1 in SMMC-7721 cells transfected with Lv-shRRS1 were significantly decreased. Further experiments found that silencing of RRS1 gene expression in SMMC-7721 cells significantly suppressed cell proliferation, inhibited colony formation capacity, increased apoptosis and arrested cells in the G1 phase. These results suggest that the RRS1 gene plays a critical role in cell proliferation, colony formation, cell apoptosis and cell cycle distribution in human HCC cells, and that silencing of RRS1 by RNAi is a promising therapeutic approach for the treatment of HCC, and should be further developed.

Indexed as

ApoptosisCarcinoma, HepatocellularCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLentivirusLiver NeoplasmsMaleNuclear ProteinsRNA-Binding ProteinsRNA InterferenceRNA, MessengerNuclear ProteinsRNA-Binding ProteinsRNA, MessengerRRS1 protein, human

Identifiers

PMID28849112
PMCPMC5652961
OpenAlexW2749959219

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.