Evidence map›Paper›PMID 26196957›Full record

ArticleScientific reports2015

Suppression of Poly(rC)-Binding Protein 4 (PCBP4) reduced cisplatin resistance in human maxillary cancer cells.

Yumi Ito, Norihiko Narita, Nozomi Nomi, Chizuru Sugimoto, Tetsuji Takabayashi, Takechiyo Yamada, Kazuhiro Karaya, Hideki Matsumoto, Shigeharu Fujieda

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

5 citing papers in PubMed, 9 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

9 authors at 2 institutions in 1 country.

Yumi ItoDepartment of Otorhinolaryngology Head and Neck Surgery, Faculty of Medical Sciences, University of Fukui, 23 Shimoaizuki, Matsuoka, Eiheiji, Fukui, 910-1193, Japan.
Norihiko NaritaDepartment of Otorhinolaryngology Head and Neck Surgery, Faculty of Medical Sciences, University of Fukui, 23 Shimoaizuki, Matsuoka, Eiheiji, Fukui, 910-1193, Japan.
Nozomi NomiDepartment of Otorhinolaryngology, Faculty of Medical Sciences, University of Oita.
Chizuru SugimotoDepartment of Otorhinolaryngology Head and Neck Surgery, Faculty of Medical Sciences, University of Fukui, 23 Shimoaizuki, Matsuoka, Eiheiji, Fukui, 910-1193, Japan.
Tetsuji TakabayashiDepartment of Otorhinolaryngology Head and Neck Surgery, Faculty of Medical Sciences, University of Fukui, 23 Shimoaizuki, Matsuoka, Eiheiji, Fukui, 910-1193, Japan.
Takechiyo YamadaDepartment of Otorhinolaryngology Head and Neck Surgery, Faculty of Medical Sciences, University of Fukui, 23 Shimoaizuki, Matsuoka, Eiheiji, Fukui, 910-1193, Japan.
Kazuhiro KarayaDivision of Bioresearch, Life Science Research Laboratory, Faculty of Medical Sciences, University of Fukui, 23 Shimoaizuki, Matsuoka, Eiheiji, Fukui, 910-1193, Japan.
Hideki MatsumotoDivision of Oncology, Biomedical Imaging Research Center, Faculty of Medical Sciences, University of Fukui, 23 Shimoaizuki, Matsuoka, Eiheiji, Fukui, 910-1193, Japan.
Shigeharu FujiedaDepartment of Otorhinolaryngology Head and Neck Surgery, Faculty of Medical Sciences, University of Fukui, 23 Shimoaizuki, Matsuoka, Eiheiji, Fukui, 910-1193, Japan.
University of Fukui · JPOita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin plays an important role in the therapy for human head and neck cancers. However, cancer cells develop cisplatin resistance, leading to difficulty in treatment and poor prognosis. To analyze cisplatin-resistant mechanisms, a cisplatin-resistant cell line, IMC-3CR, was established from the IMC-3 human maxillary cancer cell line. Flow cytometry revealed that, compared with IMC-3 cells, cisplatin more dominantly induced cell cycle G2/M arrest rather than apoptosis in IMC-3CR cells. That fact suggests that IMC-3CR cells avoid cisplatin-induced apoptosis through induction of G2/M arrest, which allows cancer cells to repair damaged DNA and survive. In the present study, we specifically examined Poly(rC)-Binding Protein 4 (PCBP4), which reportedly induces G2/M arrest. Results showed that suppression of PCBP4 by RNAi reduced cisplatin-induced G2/M arrest and enhanced apoptosis in IMC-3CR cells, resulting in the reduction of cisplatin resistance. In contrast, overexpression of PCBP4 in IMC-3 cells induced G2/M arrest after cisplatin treatment and enhanced cisplatin resistance. We revealed that PCBP4 combined with Cdc25A and suppressed the expression of Cdc25A, resulting in G2/M arrest. PCBP4 plays important roles in the induction of cisplatin resistance in human maxillary cancers. PCBP4 is a novel molecular target for the therapy of head and neck cancers, especially cisplatin-resistant cancers.

Indexed as

Apoptosiscdc25 PhosphatasesCell Line, TumorCisplatinDNA DamageDrug Resistance, NeoplasmG2 Phase Cell Cycle CheckpointsHumansMaxillary NeoplasmsM Phase Cell Cycle CheckpointsRNA-Binding ProteinsSignal TransductionCDC25A protein, humancdc25 PhosphatasesCisplatinPCBP4 protein, humanRNA-Binding Proteins

Identifiers

PMID26196957
PMCPMC4508830
OpenAlexW963135152

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.