Evidence map›Paper›PMID 32644283›Full record

ArticleCancer science2020

The catalytically defective receptor protein tyrosine kinase EphA10 promotes tumorigenesis in pancreatic cancer cells.

Won-Sik Shin, Mi Kyung Park, Young Hun Lee, Kyung Woo Kim, Ho Lee, Seung-Taek Lee

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. 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
1.8field-weighted citation impact, top 16% 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, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Eph Receptors in Cancer.Biomedicines · 2023
    Review
  9. Article
  10. Article
  11. The role of EphA7 in different tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  12. Article
  13. Article
  14. 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

6 authors at 2 institutions in 1 country.

Won-Sik ShinDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.ORCID https://orcid.org/0000-0001-9432-1320
Mi Kyung ParkDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Gyeonggi, Korea.
Young Hun LeeDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.
Kyung Woo KimDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.
Ho LeeDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Gyeonggi, Korea.
Seung-Taek LeeDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.ORCID https://orcid.org/0000-0001-7300-9784
Yonsei University · KRNational Cancer Center · KR

Funding

BK21 PLUSNational Research Foundation of Korea 2016R1A2B4007904National Research Foundation of Korea 2019M3A9A8065054
6 · The paper itself

Abstract

EphA10 (erythropoietin-producing hepatocellular carcinoma receptor A10) is a catalytically defective receptor protein tyrosine kinase in the ephrin receptor family. Although EphA10 is involved in the malignancy of some types of cancer, its role as an oncogene has not been extensively studied. Here, we investigated the influence of EphA10 on the tumorigenic potential of pancreatic cancer cells. Analysis of expression profiles from The Cancer Genome Atlas confirmed that EphA10 was elevated and higher in tumor tissues than in normal tissues in some cancer types, including pancreatic cancer. EphA10 silencing reduced the proliferation, migration, and adhesion of MIA PaCa-2 and AsPC-1 pancreatic cancer cells. These effects were reversed by overexpression of EphA10 in MIA PaCa-2 cells. Importantly, overexpression and silencing of EphA10 respectively increased and decreased the weight, volume, and number of Ki-67-positive proliferating cells in MIA PaCa-2 xenograft tumors. Further, EphA10 expression was positively correlated with invasion and gelatin degradation in MIA PaCa-2 cells. Moreover, overexpression of EphA10 enhanced the expression and secretion of MMP-9 in MIA PaCa-2 cells and increased the expression of MMP-9 and the vascular density in xenograft tumors. Finally, expression of EphA10 increased the phosphorylation of ERK, JNK, AKT, FAK, and NF-κB, which are important for cell proliferation, survival, adhesion, migration, and invasion. Therefore, we suggest that EphA10 plays a pivotal role in the tumorigenesis of pancreatic epithelial cells and is a novel therapeutic target for pancreatic cancer.

Indexed as

Disease SusceptibilityAnimalsCarcinogenesisCell AdhesionCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalGene Knockdown TechniquesHeterograftsHumansMatrix Metalloproteinase 9MicePancreatic NeoplasmsReceptors, Eph FamilySignal TransductionEPHA10 protein, humanMatrix Metalloproteinase 9Receptors, Eph FamilyEphA10pancreatic cancerreceptor protein tyrosine kinasetumorigenesisxenograft

Identifiers

PMID32644283
PMCPMC7469775
OpenAlexW3041409560

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.