Evidence map›Paper›PMID 29137316›Full record

ArticleOncotarget2017

RRS1 silencing suppresses colorectal cancer cell proliferation and tumorigenesis by inhibiting G2/M progression and angiogenesis.

Xin-Lin Wu, Zhi-Wen Yang, Li He, Pei-De Dong, Ming-Xing Hou, Xing-Kai Meng, Hai-Ping Zhao, Zhao-Yang Wang, Feng Wang, Baoluri and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

29 citing papers in PubMed, 44 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

14 authors at 1 institution in 1 country.

Xin-Lin WuDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Zhi-Wen YangDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Li HeDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Pei-De DongDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Ming-Xing HouDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Xing-Kai MengDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Hai-Ping ZhaoDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Zhao-Yang WangDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Feng WangDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
BaoluriDepartment of Pathology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
WurenqimugeDepartment of Pathology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
AgudamuDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Yong-Feng JiaDepartment of Pathology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Lin ShiDepartment of Pathology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China.
Inner Mongolia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the most common malignancies worldwide. Ribosome biogenesis regulatory protein homolog (RRS1) is an essential factor involved in ribosome biogenesis, while its role in CRC remains largely unclear. Here, we found that RRS1 expression was significantly higher in CRC tissues compared with adjacent normal tissues. RRS1 High expression also predicted poor overall survival of CRC patients. Knockdown of RRS1 induced the G2/M cell cycle arrest, apoptosis and suppressed the proliferation of RKO and HCT-116 CRC cells. Furthermore, angiogenesis was also reduced in CRC cells after RRS1 knockdown. In addition, suppression of RRS1 blunted the tumor formation of CRC cells in nude mice. At the molecular level, silencing of RRS1 decreased the expression of M-phase inducer phosphatase 3 (CDC25C), Cyclin-dependent kinase 1 (CDK1), antigen KI-67 (KI67) and increased the protein level of cyclin-dependent kinase inhibitor 1 (CDKN1A) and tumor suppressor p53 (p53). Taken together, our findings provide evidence that RRS1 may promote the development of colon cancer. Therefore, targeting RRS1 may be a promising therapeutic strategy for CRC patients.

Indexed as

angiogenesisapoptosiscell cycle arrestcolorectal cancerRRS1

Identifiers

PMID29137316
PMCPMC5669942
OpenAlexW2754478684

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.