Evidence map›Paper›PMID 33869050›Full record

ArticleFrontiers in oncology2021

Akt Inhibition Enhanced the Growth Inhibition Effects of Low-Dose Heavy-Ion Radiation

Ke Huang, Wei Zhao, Xuqiao Wang, Yingfei Qiu, Zelin Liu, Rui Chen, Wei Liu, Bin Liu

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

6 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Ke HuangSchool/Hospital of Stomatology, Lanzhou University, Lanzhou, China.
Wei ZhaoPeking University People's Hospital, Peking University, Beijing, China.
Xuqiao WangSchool/Hospital of Stomatology, Lanzhou University, Lanzhou, China.
Yingfei QiuSchool/Hospital of Stomatology, Lanzhou University, Lanzhou, China.
Zelin LiuSchool/Hospital of Stomatology, Lanzhou University, Lanzhou, China.
Rui ChenSchool/Hospital of Stomatology, Lanzhou University, Lanzhou, China.
Wei LiuLanzhou University Second Hospital, Lanzhou University, Lanzhou, China.
Bin LiuSchool/Hospital of Stomatology, Lanzhou University, Lanzhou, China.
Lanzhou University · CNLanzhou University Second Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlioma has one of the highest mortality rates of all tumors of the nervous system and commonly used treatments almost always fail to achieve tumor control. Low-dose carbon-ion radiation can effectively target cancer and tumor cells, but the mechanisms of growth inhibition induced by heavy-ion radiation

methodsCarbon-ion radiation was used to investigate the effects of heavy-ion radiation on C6 cells, and suppression of Akt was performed using perifosine. MTT assays were used to investigate optimal perifosine treatment concentrations. Clone formation assays were used to investigate the growth inhibition effects of carbon-ion radiation and the effects of radiation with Akt inhibition. Lactate dehydrogenase release, superoxide dismutase activity, and malondialdehyde content were assessed to investigate oxidative stress levels. Expression levels of proteins in the PI3K/Akt/p53 signaling pathway were assessed

resultsThe 10% maximum inhibitory concentration of perifosine was 19.95 μM. In clone formation assays there was no significant inhibition of cell growth after treatment with heavy-ion irradiation, whereas perifosine enhanced inhibition. Heavy-ion radiation induced lactate dehydrogenase release, increased the level of malondialdehyde, and reduced superoxide dismutase activity. Akt inhibition promoted these processes. Heavy-ion radiation treatment downregulated Akt expression, and upregulated B-cell lymphoma-2 (Bcl-2) expression. p53 and Bcl-2 expression were significantly upregulated, and Bcl-2-associated X protein (Bax) expression was downregulated. The expression profiles of pAkt, Bcl-2, and Bax were reversed by perifosine treatment. Caspase 3 expression was upregulated in all radiation groups.

conclusionsThe growth inhibition effects of low-dose heavy-ion irradiation were not substantial in C6 cells, and Akt inhibition induced by perifosine enhanced the growth inhibition effects

Indexed as

glioblastomagrowth inhibitionheavy-ion radiationperifosinePI3K/Akt/p53 pathway

Identifiers

PMID33869050
PMCPMC8047659
OpenAlexW3140293766

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.