Evidence map›Paper›PMID 26175934›Full record

ArticleAmerican journal of cancer research2015

OPCML is frequently methylated in human colorectal cancer and its restored expression reverses EMT via downregulation of smad signaling.

Chunhong Li, Liping Tang, Lijuan Zhao, Lili Li, Qian Xiao, Xinrong Luo, Weiyan Peng, Guosheng Ren, Qian Tao, Tingxiu Xiang

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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 35 citations in OpenAlex.

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  12. [Luteolin reverses OPCML methylation to inhibit proliferation of breast cancer MDA-MB-231 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
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  18. Cancer management and research · 2019
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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

10 authors at 3 institutions in 2 countries.

Chunhong LiMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China ; Department of Endocrine and breast Surgery, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China.
Liping TangDepartment of Gastroenterology, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China.
Lijuan ZhaoMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China.
Lili LiCancer Epigenetics Laboratory, Department of Clinical Oncology, Sir YK Pao Center for Cancer and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong and CUHK Shenzhen Research Institute Hong Kong, China.
Qian XiaoMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China.
Xinrong LuoMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China.
Weiyan PengMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China.
Guosheng RenMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China ; Department of Endocrine and breast Surgery, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China.
Qian TaoMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China ; Cancer Epigenetics Laboratory, Department of Clinical Oncology, Sir YK Pao Center for Cancer and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong and CUHK Shenzhen Research Institute Hong Kong, China.
Tingxiu XiangMolecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China.
The Affiliated Yongchuan Hospital of Chongqing Medical University · CNChinese University of Hong Kong · HKChinese University of Hong Kong, Shenzhen · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence has indicated that the expression of OPCML gene is frequently altered in a variety of cancers. We previously demonstrated that the OPCML gene is a target of epigenetic inactivation and its gene product exhibits tumor-suppressive properties. However, little is known regarding the effects and mechanisms of OPCML in colon cancer. We show that the loss or downregulation of OPCML is associated with its promoter hypermethylation. Methylation of the OPCML promoter was detected in all tumors and tumor-adjacent tissues, but lower methylation in normal colon tissues. The drug-induced release of epigenetic silencing was able to restore OPCML expression and the re-expression led to the suppression of cell growth. Furthermore, the increase in OPCML expression reversed a partial epithelial-to-mesenchymal (EMT)-like transition. Cell migration and invasiveness were also inhibited in response to OPCML upregulation. These actions were mediated through the inactivation of TGFβ-Smad signaling pathways. In addition, OPCML expression was associated with two upstream nuclear receptors (ERRa and RORa). Altogether, our study reveals OPCML as a potential tumor suppressor gene epigenetically silenced in colon cancer. Our study will help to elucidate the anti-invasive mechanisms of OPCML and establish new chemotherapeutic strategies for human colon cancer.

Indexed as

cancermethylationOPCMLTumor suppressor

Identifiers

PMID26175934
PMCPMC4497432
OpenAlexW2432996367

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.