Evidence map›Paper›PMID 33553335›Full record

ArticleAnnals of translational medicine2021

CMTM8 as an LPA1-associated partner mediates lysophosphatidic acid-induced pancreatic cancer metastasis.

Weidong Shi, Chenyue Zhang, Zhouyu Ning, Yongqiang Hua, Ye Li, Lianyu Chen, Luming Liu, Zhen Chen, Zhiqiang Meng

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Frontiers in immunology · 2026
    Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
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.

Weidong ShiDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Chenyue ZhangDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Zhouyu NingDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Yongqiang HuaDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Ye LiDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Lianyu ChenDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Luming LiuDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Zhen ChenDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Zhiqiang MengDepartment of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Shanghai Medical College of Fudan University · CNFudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLysophosphatidic acid (LPA) is known to promote cancer cell invasiveness through LPA1, but the downstream signaling cascades are still not fully clarified. The CKLF-like MARVEL transmembrane domain-containing (CMTM) family regulates aggressive phenotype in many cancers.

methodsWe performed LPA1 co-immunoprecipitation combined with mass spectrometry to search for LPA1-associated proteins. The role of CMTM8 in mediating the pro-invasive activity of LPA was investigated in pancreatic cancer.

resultsWe identified CMTM8 as an LPA1-interacting protein. LPA1 and CMTM8 were co-localized in pancreatic cancer cells. LPA treatment led to stabilization of CMTM8 protein, which was impaired by knockdown of LPA1. Depletion of CMTM8 significantly suppressed the migration and invasion of pancreatic cancer cells. Conversely, ectopic expression of CMTM8 enhanced the migratory and invasive capacity of pancreatic cancer cells. CMTM8 depletion blocked the formation of metastatic lesions in the lung. Knockdown of CMTM8 attenuated LPA-induced migration and invasion in pancreatic cancer cells. CMTM8 overexpression stimulated β-catenin activation through reduction of GSK3β. In addition, knockdown of β-catenin dramatically antagonized CMTM8-mediated migration and invasion in pancreatic cancer cells.

conclusionsCMTM8 serves as a key mediator of LPA-induced invasiveness in pancreatic cancer. The interaction between CMTM8 and LPA1 leads to activation of oncogenic β-catenin signaling. CMTM8 represents a potential therapeutic target for pancreatic cancer.

Indexed as

CKLF-like MARVEL transmembrane domain-containing 8 (CMTM8)invasionlysophosphatidic acid 1 (LPA1)pancreatic cancerβ-catenin

Identifiers

PMID33553335
PMCPMC7859753
OpenAlexW3108468735

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.