Evidence map›Paper›PMID 23070808›Full record

ArticleMolecular and cellular biochemistry2013

CCDC134 is down-regulated in gastric cancer and its silencing promotes cell migration and invasion of GES-1 and AGS cells via the MAPK pathway.

Jialing Zhong, Mei Zhao, Qing Luo, Yiming Ma, Jian Liu, Jia Wang, Mei Yang, Xinghua Yuan, Jianli Sang, Changzhi Huang

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. ER-resident CCDC134 safeguards TLR4 maturation by maintaining gp96 stability.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. A Novel Ten-Gene Signature Predicting Prognosis in Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2020
    Article
  14. Overexpression of Coiled-Coil Domain-Containing Protein 34 (CCDC34) and its Correlation with Angiogenesis in Esophageal Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  15. Article
  16. CCDC134 serves a crucial role in embryonic development.International journal of molecular medicine · 2018
    Article
  17. Expression of Coiled-Coil Domain Containing 34 (CCDC34) and its Prognostic Significance in Pancreatic Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  18. Article
  19. Review
  20. Article
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 2 institutions in 1 country.

Jialing ZhongDepartment of Etiology and Carcinogenesis and State Key Laboratory of Molecular Oncology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 17 Panjiayuan Nanli, Chaoyang District, Beijing 100021, People's Republic of China.
Mei Zhao
Qing Luo
Yiming Ma
Jian Liu
Jia Wang
Mei Yang
Xinghua Yuan
Jianli Sang
Changzhi Huang
Chinese Academy of Medical Sciences & Peking Union Medical College · CNBeijing Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CCDC134 (coiled coil domain containing 134), a novel secretory protein, acts as an inhibitor of Erk1/2 and JNK/SAPK pathways. However, the role of CCDC134 in cancer development is still lacking. In this study, we found that CCDC134 expression significantly reduced in gastric cancer tissues compared with normal tissues (P < 0.001) and lesion tissues (P < 0.001). But no statistically significant difference was observed between normal and lesion tissues (P = 0.842). In vitro transient transfection of CCDC134-specific siRNA significantly promoted the migration and invasion of both the normal gastric epithelial cell line GES-1 and gastric cancer cell line AGS cells. Further analysis revealed that the attenuated expression of CCDC134 promoted the activation of Erk1/2 and JNK/SAPK, but had no effect on p38. The activation of Erk1/2 and JNK/SAPK was required for CCDC134-mediated migration and invasion. Besides, CCDC134-RNAi could induce the expression of MMP-2 and MMP-9, which are key molecules involved in regulating cell migration and invasion. Therefore, CCDC134 may be a candidate biomarker for malignant transformation. It plays a role in regulation of cell migration and invasion, and could be a therapeutic target of gastric cancer.

Indexed as

Cell MovementMAP Kinase Signaling SystemRNA InterferenceCell LineDown-RegulationExtracellular Signal-Regulated MAP KinasesGene Knockdown TechniquesHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4Matrix Metalloproteinase 2Matrix Metalloproteinase 9Membrane ProteinsNeoplasm InvasivenessNuclear Proteinsp38 Mitogen-Activated Protein KinasesCCDC134 protein, humanExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4Matrix Metalloproteinase 2Matrix Metalloproteinase 9Membrane ProteinsMMP2 protein, humanMMP9 protein, humanNuclear Proteinsp38 Mitogen-Activated Protein KinasesRNA, Small Interfering

Identifiers

PMID23070808
OpenAlexW2082987222

What OpenQuestion holds

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Registered trials

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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.