Evidence map›Paper›PMID 24244679›Full record

ArticlePloS one2013

Annexin A4 is involved in proliferation, chemo-resistance and migration and invasion in ovarian clear cell adenocarcinoma cells.

Tae Mogami, Naho Yokota, Mikiko Asai-Sato, Roppei Yamada, Shiro Koizume, Yuji Sakuma, Mitsuyo Yoshihara, Yoshiyasu Nakamura, Yasuo Takano, Fumiki Hirahara and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Overexpression of annexin A4 indicates poor prognosis and promotes tumor metastasis of hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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  8. The role of annexins in central nervous system development and disease.Journal of molecular medicine (Berlin, Germany) · 2024
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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.

Tae MogamiMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan ; Department of Obstetrics and Gynecology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Naho Yokota
Mikiko Asai-Sato
Roppei Yamada
Shiro Koizume
Yuji Sakuma
Mitsuyo Yoshihara
Yoshiyasu Nakamura
Yasuo Takano
Fumiki Hirahara
Yohei Miyagi
Etsuko Miyagi
Kanagawa Cancer CenterYokohama City University · JPKanagawa Prefectural Hospital Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian clear cell adenocarcinoma (CCC) is the second most common subtype of ovarian cancer after high-grade serous adenocarcinomas. CCC tends to develop resistance to the standard platinum-based chemotherapy, and has a poor prognosis when diagnosed in advanced stages. The ANXA4 gene, along with its product, a Ca(++)-binding annexin A4 (ANXA4) protein, has been identified as the CCC signature gene. We reported two subtypes of ANXA4 with different isoelectric points (IEPs) that are upregulated in CCC cell lines. Although several in vitro investigations have shown ANXA4 to be involved in cancer cell proliferation, chemoresistance, and migration, these studies were generally based on its overexpression in cells other than CCC. To elucidate the function of the ANXA4 in CCC cells, we established CCC cell lines whose ANXA4 expressions are stably knocked down. Two parental cells were used: OVTOKO contains almost exclusively an acidic subtype of ANXA4, and OVISE contains predominantly a basic subtype but also a detectable acidic subtype. ANXA4 knockdown (KO) resulted in significant growth retardation and greater sensitivity to carboplatin in OVTOKO cells. ANXA4-KO caused significant loss of migration and invasion capability in OVISE cells, but this effect was not seen in OVTOKO cells. We failed to find the cause of the different IEPs of ANXA4, but confirmed that the two subtypes are found in clinical CCC samples in ratios that vary by patient. Further investigation to clarify the mechanism that produces the subtypes is needed to clarify the function of ANXA4 in CCC, and might allow stratification and improved treatment strategies for patients with CCC.

Indexed as

Adenocarcinoma, Clear CellAnnexin A4Blotting, WesternCell Line, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmExtracellular Matrix ProteinsFemaleHumansHyaluronan ReceptorsIsoelectric PointLysosomal-Associated Membrane Protein 2Ovarian NeoplasmsPrognosisAnnexin A4Extracellular Matrix Proteinshyaluronan-mediated motility receptorHyaluronan ReceptorsLAMP2 protein, humanLysosomal-Associated Membrane Protein 2

Identifiers

PMID24244679
PMCPMC3823662
OpenAlexW2074655501

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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.