Evidence map›Paper›PMID 26101717›Full record

ArticleAmerican journal of cancer research2015

MYBL2 is an independent prognostic marker that has tumor-promoting functions in colorectal cancer.

Fei Ren, Lisha Wang, Xiaohan Shen, Xiuying Xiao, Zebing Liu, Ping Wei, Yiqin Wang, Peng Qi, Chen Shen, Weiqi Sheng and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

53 citing papers in PubMed, 64 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

11 authors at 2 institutions in 1 country.

Fei RenDepartment of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Institute of Pathology, Fudan University Shanghai 200032, China.
Lisha WangDepartment of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Institute of Pathology, Fudan University Shanghai 200032, China.
Xiaohan ShenDepartment of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Institute of Pathology, Fudan University Shanghai 200032, China.
Xiuying XiaoDepartment of Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University Shanghai 200127, China.
Zebing LiuDepartment of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Institute of Pathology, Fudan University Shanghai 200032, China.
Ping WeiDepartment of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Institute of Pathology, Fudan University Shanghai 200032, China.
Yiqin WangDepartment of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Institute of Pathology, Fudan University Shanghai 200032, China.
Peng QiDepartment of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Institute of Pathology, Fudan University Shanghai 200032, China.
Chen ShenDepartment of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Institute of Pathology, Fudan University Shanghai 200032, China.
Weiqi ShengDepartment of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Institute of Pathology, Fudan University Shanghai 200032, China.
Xiang DuDepartment of Pathology, Fudan University Shanghai Cancer Center Shanghai 200032, China ; Department of Oncology, Shanghai Medical College, Fudan University Shanghai 200032, China ; Institute of Pathology, Fudan University Shanghai 200032, China ; Institutes of Biomedical Sciences, Fudan University Shanghai 200032, China.
Fudan University Shanghai Cancer Center · CNRenji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The MYBL2 gene plays an important role in the genesis and progression of tumors; however, few studies to date have defined the role of this gene in colorectal cancer (CRC). The aim of this study was to determine the relationship between MYBL2 and the prognosis of patients with CRC and to determine the possible effect of MYBL2 on colorectal carcinogenesis. Solid CRC tissues (n=180) preserved with RNAlater were collected to examine the mRNA levels of MYBL2 by real-time quantitative PCR (RT-qPCR). Formalin-fixed, paraffin-embedded (FFPE) blocks of CRC tissues (n=97) and adjacent noncancerous tissues (ANCTs, n=104) were obtained to detect MYBL2 protein levels by immunohistochemistry (IHC). siRNA was used to downregulate MYBL2 expression in the SW480 cell line to detect changes in proliferation, cell cycle progression, apoptosis, migration and invasion. The protein levels of MYBL2 were significantly higher in CRC tissues compared with ANCTs (P<0.05). Kaplan-Meier survival curves indicated that disease-free survival (DFS) was significantly worse in CRC patients in whom MYBL2 was overexpressed (at both the mRNA and protein levels) compared with patients not overexpressing MYBL2. Cox multivariate analysis revealed MYBL2 overexpression as an independent prognostic factor for poor patient survival. In addition, siRNA downregulation of MYBL2 suppressed SW480 cell proliferation, delayed cell cycle progression and induced apoptosis; however, changes in cell migration were minor. Western blot analysis demonstrated an association between MYBL2 expression and that of MMP9, Vimentin, and E-cadherin. MYBL2 is overexpressed in CRC and may therefore play an important role in tumourigenesis.

Indexed as

apoptosiscell cyclecolorectal carcinomaepithelial to mesenchymal transitionMYBL2prognosisproliferation

Identifiers

PMID26101717
PMCPMC4473330
OpenAlexW772610701

What OpenQuestion holds

Textmetadata
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.