Evidence map›Paper›PMID 27669982›Full record

ArticleJournal of experimental & clinical cancer research : CR2016

TLE3 represses colorectal cancer proliferation by inhibiting MAPK and AKT signaling pathways.

Run-Wei Yang, Ying-Yue Zeng, Wen-Ting Wei, Yan-Mei Cui, Hui-Ying Sun, Yue-Long Cai, Xin-Xin Nian, Yun-Teng Hu, Yu-Ping Quan, Sheng-Lu Jiang and 9 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 15% 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, 20 citations in OpenAlex.

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  9. Transducin-Like Enhancer of Split 3 (TLE3) Expression Is Associated with Taxane Sensitivity in Nonserous Ovarian Carcinoma in a Three-Cohort Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 3 institutions in 1 country.

Run-Wei YangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Ying-Yue ZengDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Wen-Ting WeiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Yan-Mei CuiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Hui-Ying SunDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Yue-Long CaiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Xin-Xin NianDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Yun-Teng HuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Yu-Ping QuanDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Sheng-Lu JiangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Meng WangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Ya-Li ZhaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Jun-Feng QiuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Ming-Xuan LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Jia-Huan ZhangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Mei-Rong HeGuangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Li LiangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Yan-Qing DingDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China. dyq@fimmu.com.
Wen-Ting LiaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China. liaowt2002@gmail.com.
Nanfang Hospital · CNSouthern Medical University · CNKey Laboratory of Guangdong Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTransducin-like enhancer of Split3 (TLE3) serves as a transcriptional corepressor during cell differentiation and shows multiple roles in different kinds of cancers. Recently, TLE3 together with many other genes involved in Wnt/β-catenin pathway were detected hyper-methylated in colorectal cancer (CRC). However, the potential role and the underlying mechanism of TLE3 in CRC progression remain scarce.

methodsGene expression profiles were analyzed in The Cancer Genome Atlas (TCGA) microarray dataset of 41 normal colorectal intestine tissues and 465 CRC tissues. Western blot and Real-time Quantitative PCR (RT-qPCR) were respectively performed to detect protein and mRNA expression in 8 pairs of CRC tissue and matched adjacent normal mucosa. Immunohistochemistry (IHC) was conducted to evaluate TLE3 protein expression in 105 paraffin-embedded, archived human CRC tissues from patients, whose survival data were analyzed with Kaplan-Meier method. In vitro experiments including MTT assay, colony formation assay, and soft agar formation assay were used to investigate the effects of TLE3 on CRC cell growth and proliferation. Additionally, subcutaneous tumorigenesis assay was performed in nude mice to confirm the effects of TLE3 in vivo. Furthermore, gene set enrichment analysis (GSEA) was run to explore potential mechanism of TLE3 in CRC, and then we measured the distribution of CRC cell cycle phases and apoptosis by flow cytometry, as well as the impacts of TLE3 on MAPK and AKT signaling pathways by Western blot and RT-qPCR.

resultsTLE3 was significantly down-regulated in 465 CRC tissues compared with 41 normal tissues. Both protein and mRNA expressions of TLE3 were down-regulated in CRC compared with matched adjacent normal mucosa. Lower expression of TLE3 was significantly associated with poorer survival of patients with CRC. Besides, knock down of TLE3 promoted CRC cell growth and proliferation, while overexpression of TLE3 showed suppressive effects. Furthermore, overexpression of TLE3 caused G1-S phase transition arrest, inhibition of MAPK and AKT pathways, and up-regulation of p21Cip1/WAF1 and p27Kip1.

conclusionThis study indicated that TLE3 repressed CRC proliferation partly through inhibition of MAPK and AKT signaling pathways, suggesting the possibility of TLE3 as a biomarker for CRC prognosis.

Indexed as

Colorectal cancerp21Cip1/WAF1p27Kip1PrognosisProliferationTLE3

Identifiers

PMID27669982
PMCPMC5037636
OpenAlexW2527248094

What OpenQuestion holds

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LicenceCC BY
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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.