Evidence map›Paper›PMID 25862630›Full record

ArticleHuman cell2015

Enhanced sensitivity to sorafenib by inhibition of Akt1 expression in human renal cell carcinoma ACHN cells both in vitro and in vivo.

Hiromoto Tei, Hideaki Miyake, Masato Fujisawa

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 13 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

3 authors at 1 institution in 1 country.

Hiromoto TeiDivision of Urology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Hideaki Miyake
Masato Fujisawa
Kobe University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate whether antitumor activity of sorafenib, a potential molecular-targeted agent against RCC is enhanced by silencing Akt1 in a human RCC ACHN model. We established ACHN in which the expression vector containing short hairpin RNA targeting Akt1 was introduced (ACHN/sh-Akt1). Changes in several phenotypes of ACHN/sh-Akt1 following treatment with sorafenib were compared with those of ACHN transfected with control vector alone (ACHN/C) both in vitro and in vivo. When cultured in the standard medium, there was no significant difference in the in vitro growth pattern between ACHN/sh-Akt1 and ACHN/C; however, compared with ACHN/C, ACHN/sh-Akt1 showed a significantly higher sensitivity to sorafenib. Furthermore, treatment with Akt1 inhibitor, A-674563 also resulted in the significantly enhanced sensitivity of parental ACHN to sorafenib. Treatment of ACHN/sh-Akt1 with sorafenib, but not that of ACHN/C, induced marked downregulation of antiapoptotic proteins, including Bcl-2, Bcl-xL, and c-Myc. In vivo administration of sorafenib resulted in the significant growth inhibition of ACHN/sh-Akt1 tumor compared with that of ACHN/C tumor, and despite the lack of Ki-67 labeling index between ACHN/sh-Akt1 and ACHN/C tumors, apoptotic index in ACHN/sh-Akt1 tumor in mice treated with sorafenib was significantly greater than that in ACHN/C tumor. These findings suggest that combined treatment with Akt1 inhibitor and sorafenib could be a promising therapeutic approach for patients with advanced RCC.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarcinoma, Renal CellCell ProliferationDose-Response Relationship, DrugGene ExpressionGene SilencingHumansKidney NeoplasmsMaleMice, Inbred BALB CMice, NudeNeoplasm TransplantationNiacinamidePhenylurea CompoundsAKT1 protein, humanAntineoplastic AgentsNiacinamidePhenylurea CompoundsProto-Oncogene Proteins c-aktSorafenib

Identifiers

PMID25862630
OpenAlexW2056239152

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.