Evidence map›Paper›PMID 27919290›Full record

ArticleJournal of experimental & clinical cancer research : CR2016

CCDC88A, a prognostic factor for human pancreatic cancers, promotes the motility and invasiveness of pancreatic cancer cells.

Aki Tanouchi, Keisuke Taniuchi, Mutsuo Furihata, Seiji Naganuma, Ken Dabanaka, Masashi Kimura, Ryohei Watanabe, Takuhiro Kohsaki, Takahiro Shimizu, Motoaki Saito and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

Aki TanouchiDepartment of Gastroenterology and Hepatology; Kochi Medical School, Kochi University, Kochi, Japan. jm-tanouchi@kochi-u.ac.jp.
Keisuke TaniuchiDepartment of Gastroenterology and Hepatology; Kochi Medical School, Kochi University, Kochi, Japan.
Mutsuo FurihataDepartment of Pathology, Kochi Medical School, Kochi University, Kochi, Japan.
Seiji NaganumaDepartment of Pathology, Kochi Medical School, Kochi University, Kochi, Japan.
Ken DabanakaDepartment of Surgery, Kochi Medical School, Kochi University, Kochi, Japan.
Masashi KimuraDepartment of Surgery, Matsuyama Shimin Hospital, Matsuyama, Japan.
Ryohei WatanabeDepartment of Surgery, Matsuyama Shimin Hospital, Matsuyama, Japan.
Takuhiro KohsakiDepartment of Gastroenterology and Hepatology; Kochi Medical School, Kochi University, Kochi, Japan.
Takahiro ShimizuDepartment of Pharmacology, Kochi Medical School, Kochi University, Kochi, Japan.
Motoaki SaitoDepartment of Pharmacology, Kochi Medical School, Kochi University, Kochi, Japan.
Kazuhiro HanazakiDepartment of Surgery, Kochi Medical School, Kochi University, Kochi, Japan.
Toshiji SaibaraDepartment of Gastroenterology and Hepatology; Kochi Medical School, Kochi University, Kochi, Japan.
Kōchi University · JPMatsuyama Shimin Hospital · JPKochi Medical School Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCoiled-Coil Domain Containing 88A (CCDC88A) was identified as a substrate of the serine/threonine kinase Akt that is capable of binding to the actin cytoskeleton. The aim of this study was to investigate the potential role of CCDC88A in the migration and invasiveness of pancreatic ductal adenocarcinoma (PDAC) cells.

methodsImmunohistochemistry was performed to determine whether high CCDC88A expression in human PDAC tissues is correlated with poor prognosis. Immunoprecipitation, immunoblotting and immunocytochemistry were performed to determine the intracellular distribution of CCDC88A, and its association with the serine/threonine kinase Akt and actin-filaments in PDAC cells. Phosphoprotein array analysis was performed to determine CCDC88A-associated intracellular signaling pathways. Finally, immunofluorescence analyses and Matrigel invasion assays were performed to examine the effects of CCDC88A on the formation of cell protrusions and PDAC cell invasion.

resultsExpression of CCDC88A in PDAC tissue was significantly correlated with overall survival. CCDC88A was co-localized with peripheral actin structures in cell protrusions of migrating PDAC cells. Knockdown of CCDC88A inhibited the migration and invasiveness of PDAC cells through a decrease in cell protrusions. Although CCDC88A has been previously reported to be a binding partner and substrate of Akt, the level of active Akt was not associated with the translocation of CCDC88A towards cell protrusions. CCDC88A-dependent promotion of cell migration and invasiveness was not modulated by Akt signaling. Knockdown of CCDC88A decreased phosphorylated Src and ERK1/2 and increased phosphorylated AMPK1 in PDAC cells. Knockdown of AMPK1 inhibited the migration and invasiveness of PDAC cells. The combined data suggest that CCDC88A may be a useful marker for predicting the outcome of patients with PDAC and that CCDC88A can promote PDAC cell migration and invasion through a signaling pathway that involves phosphorylation of Src and ERK1/2 and/or dephosphorylation of AMPK1.

conclusionsCCDC88A was accumulated in cell protrusions, contributed to the formation of membrane protrusions, and increased the migration and invasiveness of PDAC cells.

Indexed as

Up-RegulationAdultAgedAged, 80 and overCarcinoma, Pancreatic DuctalCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansMaleMicrofilament ProteinsMiddle AgedNeoplasm InvasivenessNeoplasm StagingPancreatic NeoplasmsCCDC88A protein, humanMicrofilament ProteinsPhosphoproteinsProto-Oncogene Proteins c-aktVesicular Transport ProteinsAkt-binding proteinAMPK1Cell invasionCell protrusionsPancreatic cancer

Identifiers

PMID27919290
PMCPMC5139074
OpenAlexW2560670377

What OpenQuestion 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 OpenQuestion graph.