Evidence map›Paper›PMID 26474560›Full record

ArticleJournal of experimental & clinical cancer research : CR2015

CMTM4 is frequently downregulated and functions as a tumour suppressor in clear cell renal cell carcinoma.

Ting Li, Yingying Cheng, Pingzhang Wang, Wenyan Wang, Fengzhan Hu, Xiaoning Mo, Hongxia Lv, Tao Xu, Wenling Han

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 57 citations in OpenAlex.

  1. Translational cancer research · 2025
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  4. Small extracellular vesicles (sEVs) in pancreatic cancer progression and diagnosis.Journal of controlled release : official journal of the Controlled Release Society · 2025
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  10. CMTM4 inhibits gastric tumorigenesis and metastasis.Journal of gastrointestinal oncology · 2024
    Article
  11. Review
  12. [Advances in the Study of Chemokine-like Factor Superfamily Members in Tumors].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
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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

9 authors at 2 institutions in 1 country.

Ting LiPeking University Center for Human Disease Genomics, Department of Immunology, Key Laboratory of Medical Immunology, Ministry of Health, School of Basic Medical Sciences, Peking University Center for Human Disease Genomics, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China. tingfanta@163.com.
Yingying ChengPeking University Center for Human Disease Genomics, Department of Immunology, Key Laboratory of Medical Immunology, Ministry of Health, School of Basic Medical Sciences, Peking University Center for Human Disease Genomics, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China. chengyingying1987@163.com.
Pingzhang WangPeking University Center for Human Disease Genomics, Department of Immunology, Key Laboratory of Medical Immunology, Ministry of Health, School of Basic Medical Sciences, Peking University Center for Human Disease Genomics, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China. wangpzh@bjmu.edu.cn.
Wenyan WangPeking University Center for Human Disease Genomics, Department of Immunology, Key Laboratory of Medical Immunology, Ministry of Health, School of Basic Medical Sciences, Peking University Center for Human Disease Genomics, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China. wywang@bjmu.edu.cn.
Fengzhan HuDepartment of Urology, Peking University People's Hospital, 11 Xi-Zhi-Men South Street, Beijing, 100044, China. guyue0910@163.com.
Xiaoning MoPeking University Center for Human Disease Genomics, Department of Immunology, Key Laboratory of Medical Immunology, Ministry of Health, School of Basic Medical Sciences, Peking University Center for Human Disease Genomics, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China. moxiaoning@bjmu.edu.cn.
Hongxia LvPeking University Center for Human Disease Genomics, Department of Immunology, Key Laboratory of Medical Immunology, Ministry of Health, School of Basic Medical Sciences, Peking University Center for Human Disease Genomics, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China. lvhongxia@yshbio.com.
Tao XuDepartment of Urology, Peking University People's Hospital, 11 Xi-Zhi-Men South Street, Beijing, 100044, China. xutao@medmail.com.cn.
Wenling HanPeking University Center for Human Disease Genomics, Department of Immunology, Key Laboratory of Medical Immunology, Ministry of Health, School of Basic Medical Sciences, Peking University Center for Human Disease Genomics, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China. hanwl@bjmu.edu.cn.
Peking University · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family (CMTM) is a gene family involved in multiple malignancies. CMTM4 is a member of this family and is located at chromosome 16q22.1, a locus that harbours a number of tumour suppressor genes. It has been defined as a regulator of cell cycle and division in HeLa cells; however, its roles in tumourigenesis remain poorly studied.

methodsAn integrated bioinformatics analysis based on the array data from the GEO database was conducted to view the differential expression of CMTM4 across multiple cancers and their corresponding control tissues. Primary clear cell renal cell carcinoma (ccRCC) and the paired adjacent non-tumour tissues were then collected to examine the expression of CMTM4 by western blotting, immunohistochemistry, and quantitative RT-PCR. The ccRCC cell lines A498 and 786-O and the normal renal tubular epithelial cell line HK-2 were also tested for CMTM4 expression by western blotting. Cell Counting Kit-8 (CCK-8) and viable cell counting assays were used to delineate the growth curves of 786-O cells after CMTM4 overexpression or knockdown. Wound healing and transwell assays were performed to assess the cells' ability to migrate. The effects of CMTM4 on cellular apoptosis and cell cycle progression were analysed by flow cytometry, and cell cycle hallmarks were detected by western blotting and RT-PCR. The xenograft model in nude mice was used to elucidate the function of CMTM4 in tumourigenesis ex vivo.

resultsBy omic data analysis, we found a substantial downregulation of CMTM4 in ccRCC. Western blotting then confirmed that CMTM4 was dramatically reduced in 86.9 % (53/61) of ccRCC tissues compared with the paired adjacent non-tumour tissues, as well as in the 786-O and A498 ccRCC cell lines. Restoration of CMTM4 significantly suppressed 786-O cell growth by inducing G2/M cell cycle arrest and p21 upregulation, and cell migration was also inhibited. However, knockdown of CMTM4 led to a completely opposite effect on these cell behaviours. Overexpression of CMTM4 also markedly inhibited the tumour xenograft growth in nude mice.

conclusionsCMTM4 is downregulated and exhibits tumour-suppressor activities in ccRCC, and could be exploited as a target for ccRCC treatment.

Indexed as

Genes, Tumor SuppressorAdultAgedAnimalsApoptosisCarcinoma, Renal CellCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticCyclin-Dependent Kinase Inhibitor p21Down-RegulationFemaleG2 Phase Cell Cycle CheckpointsHumansKidney NeoplasmsCMTM4 protein, humanCyclin-Dependent Kinase Inhibitor p21MARVEL Domain-Containing ProteinsRNA, Small InterferingTumor Suppressor Proteins

Identifiers

PMID26474560
PMCPMC4609138
OpenAlexW2140323498

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.