Evidence map›Paper›PMID 28418860›Full record

ArticleOncotarget2017

Targeting the overexpressed ROC1 induces G2 cell cycle arrest and apoptosis in esophageal cancer cells.

Jingyang Zhang, Shuo Li, Zhaoyang Shang, Shan Lin, Peng Gao, Yi Zhang, Shuaiheng Hou, Saijun Mo, Wenbo Cao, Ziming Dong and 2 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

13 citing papers in PubMed, 15 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

12 authors at 1 institution in 1 country.

Jingyang ZhangCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Shuo LiCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Zhaoyang ShangCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Shan LinCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Peng GaoCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Yi ZhangCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Shuaiheng HouCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Saijun MoCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Wenbo CaoCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Ziming DongCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Tao HuCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Ping ChenCollege of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China.
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent reports showed that regulator of Cullins-1 (ROC1) play an important role in tumor progression in a tumor-specific manner. However, the role and mechanism of ROC1 in esophageal cancer remains elusive. Here we demonstrated that ROC1 was overexpressed in esophageal squamous cell carcinomas, which was positive associated with poor prognosis of esophageal cancer patients. ROC1 knockdown significantly inhibited the growth of esophageal cancer cells in vitro and in vivo. Mechanistically, ROC1 silencing induced G2 cell cycle arrest and triggered apoptosis by accumulating the pro-apoptotic protein NOXA. Consistently, the downregulation of NOXA expression via siRNA substantially attenuated apoptosis induced by ROC1 silencing. These findings suggest that ROC1 is an appealing drug target for esophageal cancer.

Indexed as

ApoptosisG2 Phase Cell Cycle CheckpointsAnimalsCarcinoma, Squamous CellCarrier ProteinsCell Cycle ProteinsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Disease ProgressionEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaEsophagusFemaleGene Knockdown TechniquesCarrier ProteinsCDKN1A protein, humanCDKN1B protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Nuclear ProteinsPMAIP1 protein, humanProtein-Tyrosine KinasesProto-Oncogene Proteins c-bcl-2RBX1 protein, humanRNA, Small InterferingWEE1 protein, humanapoptosiscell cycleesophageal cancerNOXAROC1

Identifiers

PMID28418860
PMCPMC5438718
OpenAlexW2595030032

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.