Evidence map›Paper›PMID 32354885›Full record

ArticleIn vivo (Athens, Greece)

Enhanced Sensitivity to NVP-BEZ235 by Inhibition of p62/SQSTM1 in Human Bladder Cancer KoTCC-1 Cells Both

Keita Tamura, Kyohei Watanabe, Yuto Matsushita, Hiromitsu Watanabe, Daisuke Motoyama, Toshiki Ito, Takayuki Sugiyama, Atsushi Otsuka, Hideaki Miyake

Open access · diamondAbstract read
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. p62: Friend or Foe? Evidences forInternational journal of molecular sciences · 2020
    Review
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 1 institution in 1 country.

Keita TamuraDepartment of Urology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Kyohei WatanabeDepartment of Urology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Yuto MatsushitaDepartment of Urology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hiromitsu WatanabeDepartment of Urology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Daisuke MotoyamaDepartment of Urology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Toshiki ItoDepartment of Urology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Takayuki SugiyamaDepartment of Urology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Atsushi OtsukaDepartment of Urology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hideaki MiyakeDepartment of Urology, Hamamatsu University School of Medicine, Hamamatsu, Japan hideakimiyake@hotmail.com.
Hamamatsu University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimThe prognosis of patients with invasive bladder cancer remains poor. The objective of this study was to evaluate the efficacy of NVP-BEZ235 (NVP), a dual PI3K/mTOR inhibitor, combined with the inactivation of p62/SQSTM1 (p62) in a human bladder cancer KoTCC-1 model. MATERIALS AND

methodsAn expression plasmid with short hairpin RNA targeted against p62 was transfected into KoTCC-1 cells (KoTCC-1/sh-p62). The antitumor effects of NVP on KoTCC-1/sh-p62 were investigated in comparison with those on KoTCC-1 transfected with a control plasmid alone (KoTCC-1/C).

resultsKoTCC-1/sh-p62 showed significantly higher sensitivity to NVP than KoTCC-1/C. Treatment of both cell lines with NVP markedly inactivated the PI3K/Akt/mTOR signaling pathway. However, NVP treatment stimulated the autophagic pathway in KoTCC-1/C, but not in KoTCC-1/sh-p62. Furthermore, compared with KoTCC-1/C, NVP treatment induced apoptosis of KoTCC-1/sh-p62 cells, which was accompanied by significant downregulation of c-IAP-1 and XIAP as well as upregulation of Bax. Moreover, the in vivo growth of KoTCC-1/sh-p62 tumors was significantly suppressed by treatment with NVP compared to KoTCC-1/C tumors.

conclusionInhibition of p62 expression combined with NVP may represent an effective therapeutic approach for patients with invasive bladder cancer.

Indexed as

Drug Resistance, NeoplasmAnimalsCell Line, TumorGene ExpressionHumansImmunohistochemistryMaleMicePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsSequestosome-1 ProteinSignal TransductionTOR Serine-Threonine KinasesUrinary Bladder NeoplasmsXenograft Model Antitumor AssaysMTOR protein, humanPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsSequestosome-1 ProteinSQSTM1 protein, humanTOR Serine-Threonine Kinasesbladder cancerNVP-BEZ235p62/SQSTM1

Identifiers

PMID32354885
PMCPMC7279813
OpenAlexW3023215791

What OpenQuestion holds

Textmetadata
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.