Evidence map›Paper›PMID 34560882›Full record

ArticleCancer cell international2021

CMTM3 suppresses chordoma progress through EGFR/STAT3 regulated EMT and TP53 signaling pathway.

Wanqiong Yuan, Feng Wei, Hanqiang Ouyang, Xiaoqing Ren, Jing Hang, Xiaoning Mo, Zhongjun Liu

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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  10. [Advances in the Study of Chemokine-like Factor Superfamily Members in Tumors].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023
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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

7 authors at 2 institutions in 4 countries.

Wanqiong YuanDepartment of Orthopedics, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing, 100191, China.
Feng WeiDepartment of Orthopedics, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing, 100191, China.
Hanqiang OuyangDepartment of Orthopedics, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing, 100191, China.
Xiaoqing RenDepartment of Pharmacy, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing, China.
Jing Hang *Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Beijing, China. hangjbysy@163.com.
Xiaoning Mo *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, Haidian District, Beijing, 100191, China. moxiaoning@bjmu.edu.cn.
Zhongjun Liu *Department of Orthopedics, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing, 100191, China. zjliu@bjmu.edu.cn.ORCID http://orcid.org/0000-0003-4249-7409
Peking University · CNMinistry of Education of the People's Republic of China · CN

Funding

Beijing Natural Science Foundation 7204327Capital's Funds for Health Improvement and Research 2020-4-40916Key Clinical Projects of Peking University Third Hospital BYSYZD2019041National Key R&D Program of China 2018YFC1003702National Key R&D Program of China 2018YFC1004403National Natural Science Foundation of China 81803095
6 · The paper itself

Abstract

backgroundChordomas are rare, slow-growing and locally aggressive bone sarcomas. At present, chordomas are difficult to manage due to their high recurrence rate, metastasis tendency and poor prognosis. The underlying mechanisms of chordoma tumorigenesis and progression urgently need to be explored to find the effective therapeutic targets. Our previous data demonstrates that EGFR plays important roles in chordoma development and CKLF-like MARVEL transmembrane domain containing (CMTM)3 suppresses gastric cancer metastasis by inhibiting the EGFR/STAT3/EMT signaling pathway. However, the roles and mechanism of CMTM3 in chordomas remain unknown.

methodsPrimary chordoma tissues and the paired adjacent non-tumor tissues were collected to examine the expression of CMTM3 by western blot. The expression of CMTM3 in chordoma cell lines was tested by Real-time PCR and western blot. CCK-8 and colony forming unit assay were performed to delineate the roles of CMTM3 in cell proliferation. Wound healing and Transwell assays were performed to assess cell migration and invasion abilities. A xenograft model in NSG mice was used to elucidate the function of CMTM3 in vivo. Signaling pathways were analyzed by western blot and IHC. RNA-seq was performed to further explore the mechanism regulated by CMTM3 in chordoma cells.

resultsCMTM3 expression was downregulated in chordoma tissues compared with paired normal tissues. CMTM3 suppressed proliferation, migration and invasion of chordoma cells in vitro and inhibited tumor growth in vivo. CMTM3 accelerated EGFR degradation, suppressed EGFR/STAT3/EMT signaling pathway, upregulated TP53 expression and enriched the TP53 signaling pathway in chordoma cells.

conclusionsCMTM3 inhibited tumorigenesis and development of chordomas through activating the TP53 signaling pathway and suppressing the EGFR/STAT3 signaling pathway, which suppressed EMT progression. CMTM3 might be a potential therapeutic target for chordomas.

Indexed as

ChordomaCMTM3EGFRSTAT3TP53

Identifiers

PMID34560882
PMCPMC8461898
OpenAlexW3199952950

What Socratic 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 Socratic graph.