Evidence map›Paper›PMID 36980764›Full record

ArticleCancers2023

CCR7 Mediates Cell Invasion and Migration in Extrahepatic Cholangiocarcinoma by Inducing Epithelial-Mesenchymal Transition.

Mitsunobu Oba, Yoshitsugu Nakanishi, Tomoko Mitsuhashi, Katsunori Sasaki, Kanako C Hatanaka, Masako Sasaki, Ayae Nange, Asami Okumura, Mariko Hayashi, Yusuke Yoshida and 14 more

Full text read
In one paragraph

Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Pharmaceuticals (Basel, Switzerland) · 2024
    Article
  6. 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

24 authors.

Mitsunobu ObaDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Yoshitsugu NakanishiDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.ORCID 0000-0001-9300-7751
Tomoko MitsuhashiDepartment of Surgical Pathology, Hokkaido University Hospital, Sapporo 060-8648, Japan.
Katsunori SasakiDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Kanako C HatanakaResearch Division of Genome Companion Diagnostics, Hokkaido University Hospital, Sapporo 060-8648, Japan.
Masako SasakiNB Health Laboratory Co. Ltd., Sapporo 001-0021, Japan.
Ayae NangeResearch Division of Genome Companion Diagnostics, Hokkaido University Hospital, Sapporo 060-8648, Japan.
Asami OkumuraResearch Division of Genome Companion Diagnostics, Hokkaido University Hospital, Sapporo 060-8648, Japan.
Mariko HayashiDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Yusuke YoshidaDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Takeo NittaDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Takashi UenoDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Toru YamadaDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Masato OnoDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Shota KuwabaraDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Keisuke OkamuraDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Takahiro TsuchikawaDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.ORCID 0000-0002-3847-280X
Toru NakamuraDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Takehiro NojiDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.ORCID 0000-0003-3048-0685
Toshimichi AsanoDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.
Kimitaka TanakaDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.ORCID 0000-0001-9899-4581
Kiyoshi TakayamaNB Health Laboratory Co. Ltd., Sapporo 001-0021, Japan.
Yutaka HatanakaResearch Division of Genome Companion Diagnostics, Hokkaido University Hospital, Sapporo 060-8648, Japan.ORCID 0000-0003-3128-1477
Satoshi HiranoDepartment of Gastroenterological Surgery II, Hokkaido University Faculty of Medicine, Sapporo 060-8638, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epithelial-mesenchymal transition (EMT) contributes to the metastatic cascade in various tumors. C-C chemokine receptor 7 (CCR7) interacts with its ligand, chemokine (C-C motif) ligand 19 (CCL19), to promote EMT. However, the association between EMT and CCR7 in extrahepatic cholangiocarcinoma (EHCC) remains unknown. This study aimed to elucidate the prognostic impact of CCR7 expression and its association with clinicopathological features and EMT in EHCC. The association between CCR7 expression and clinicopathological features and EMT status was examined via the immunohistochemical staining of tumor sections from 181 patients with perihilar cholangiocarcinoma. This association was then investigated in TFK-1 and EGI-1 EHCC cell lines. High-grade CCR7 expression was significantly associated with a large number of tumor buds, low E-cadherin expression, and poor overall survival. TFK-1 showed CCR7 expression, and Western blotting revealed E-cadherin downregulation and vimentin upregulation in response to CCL19 treatment. The wound healing and Transwell invasion assays revealed that the activation of CCR7 by CCL19 enhanced the migration and invasion of TFK-1 cells, which were abrogated by a CCR7 antagonist. These results suggest that a high CCR7 expression is associated with an adverse postoperative prognosis via EMT induction and that CCR7 may be a potential target for adjuvant therapy in EHCC.

Indexed as

CCL19CCR7epithelial–mesenchymal transitionextrahepatic cholangiocarcinomatumor budding

Identifiers

PMID36980764
PMCPMC10047000

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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.