Evidence map›Paper›PMID 33757532›Full record

ArticleJournal of translational medicine2021

CMTM6 promotes migration, invasion, and EMT by interacting with and stabilizing vimentin in hepatocellular carcinoma cells.

Xiaoting Huang, Leyang Xiang, Baiyao Wang, Jijie Hu, Chunshan Liu, Anbang Ren, Kunpeng Du, Gengtai Ye, Yingying Liang, Yunqiang Tang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.9field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

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  4. [Effect of CMTM6 on PD-L1 inBeijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025
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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 3 institutions in 1 country.

Xiaoting Huang *Department of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, No. 78 Hengzhigang Road, Guangzhou, 510095, Guangdong, People's Republic of China.
Leyang Xiang *Department of Surgery, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, No. 78 Hengzhigang Road, Guangzhou, 510095, Guangdong, People's Republic of China.
Baiyao WangDepartment of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, No. 78 Hengzhigang Road, Guangzhou, 510095, Guangdong, People's Republic of China.
Jijie HuDepartment of Orthopaedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Chunshan LiuDepartment of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, No. 78 Hengzhigang Road, Guangzhou, 510095, Guangdong, People's Republic of China.
Anbang RenDepartment of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, No. 78 Hengzhigang Road, Guangzhou, 510095, Guangdong, People's Republic of China.
Kunpeng DuDepartment of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, No. 78 Hengzhigang Road, Guangzhou, 510095, Guangdong, People's Republic of China.
Gengtai YeUnit of Hepatobiliary Surgery, Department of General Surgery, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Baiyun District, Guangzhou, 510515, China.
Yingying LiangDepartment of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, No. 78 Hengzhigang Road, Guangzhou, 510095, Guangdong, People's Republic of China.
Yunqiang TangDepartment of Surgery, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, No. 78 Hengzhigang Road, Guangzhou, 510095, Guangdong, People's Republic of China. gyzl_tang@126.com.
Dinghua YangUnit of Hepatobiliary Surgery, Department of General Surgery, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Baiyun District, Guangzhou, 510515, China. dhyangyd@yahoo.com.
Yawei YuanDepartment of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, No. 78 Hengzhigang Road, Guangzhou, 510095, Guangdong, People's Republic of China. yuanyawei@gzhmu.edu.cn.
Guangzhou Medical University · CNNanfang Hospital · CNState Key Laboratory of Respiratory Disease · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCKLF like MARVEL transmembrane domain containing 6 (CMTM6) has been associated with the development in many kinds of cancers. However, the roles of CMTM6 in hepatocellular carcinoma (HCC) are largely unknown. Thus, the present study aimed to investigate the function of CMTM6 in HCC.

methodsWe analysed CMTM6 levels and functions using human HCC cell lines, paired HCC and adjacent non-tumorous tissues, and a tissue microarray. CMTM6 expression was silenced using short hairpin RNAs and its was overexpressed from a lentivirus vector. CMTM6 mRNA and protein levels were determined using quantitative real-time reverse transcription PCR and western blotting, respectively. Proliferation, colony formation, migration, and invasion were assessed using a Cell counting kit-8, colony formation, wound-healing, and Matrigel invasion assays, respectively. Immunohistochemistry was used to score the expression of CMTM6 in tissue samples. The localization and binding partners of CMTM6 were investigated using immunofluorescence and coimmunoprecipitation experiments, respectively. A mouse xenograft model was used for in vivo studies.

resultsCompared with that in adjacent, non-cancerous tissue, Here, CMTM6 levels were increased in HCC tissue samples. Silencing of CMTM6 suppressed the proliferation, migration, and invasion of HCC cells. Conversely, CMTM6 overexpression enhanced HCC cell invasion, migration, and proliferation. Mechanistically, CMTM6 physically interacts with and stabilizes vimentin, thus inducing epithelial-mesenchymal transition (EMT), which promotes proliferation, migration and invasion. Importantly, in HCC tissues, CMTM6 expression correlated positively with vimentin levels. Poor prognosis of HCC was associated significantly with higher CMTM6 expression.

conclusionsCMTM6 has an important function in HCC proliferation, migration, and invasion, via its interaction with and stabilization of vimentin. CMTM6 might represent a potential biomarker and therapeutic target to treat HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticMiceVimentinVimentinCMTM6EMTHCCInvasionMigrationProliferation

Identifiers

PMID33757532
PMCPMC7989033
OpenAlexW3127162076

What OpenQuestion holds

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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.