Evidence map›Paper›PMID 34665844›Full record

ArticlePloS one2021

PKI-587 enhances radiosensitization of hepatocellular carcinoma by inhibiting the PI3K/AKT/mTOR pathways and DNA damage repair.

Yinghai Xie, Changwei Liu, Yinci Zhang, Amin Li, Chong Sun, Rui Li, Yingru Xing, Minghong Shi, Qi Wang

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

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

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  7. The stage-dependent prognostic role ofTranslational cancer research · 2023
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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 1 institution in 1 country.

Yinghai XieHuainan First People's Hospital and First Affiliated Hospital of Medical School, Anhui University of Science and Technology, Huainan, China.
Changwei LiuHuainan First People's Hospital and First Affiliated Hospital of Medical School, Anhui University of Science and Technology, Huainan, China.
Yinci ZhangMedical School, Anhui University of Science and Technology, Huainan, China.
Amin LiMedical School, Anhui University of Science and Technology, Huainan, China.
Chong SunHuainan First People's Hospital and First Affiliated Hospital of Medical School, Anhui University of Science and Technology, Huainan, China.
Rui LiHuainan First People's Hospital and First Affiliated Hospital of Medical School, Anhui University of Science and Technology, Huainan, China.
Yingru XingAffiliated Cancer Hospital, Anhui University of Science and Technology, Huainan, China.
Minghong ShiAffiliated Cancer Hospital, Anhui University of Science and Technology, Huainan, China.
Qi WangHuainan First People's Hospital and First Affiliated Hospital of Medical School, Anhui University of Science and Technology, Huainan, China.ORCID 0000-0003-2000-5725
Anhui University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiation is an important therapeutic strategy for hepatocellular (HCC). In this study, we evaluated the role of the dual PI3K/mTOR inhibitor, PKI-587, on radiosensitization of HCC and its possible mechanism. MTT, colony formation, flow cytometry, and immunofluorescence were used to analyze the proliferation, cell cycle, formation of residual γ-H2AX foci, and apoptosis of HCC cells. A SK-Hep1 xenograft HCC model was used to assess the effects of PKI-587 in combination with ionizing radiation in vivo. The activation levels of PI3K/AKT/mTOR and DNA damage repair pathways and their downstream effector molecules were detected with Western blot. It was found that PKI-587 sensitized HCC cells to radiation by increasing DNA damage, enhancing G0/G1 cell-cycle arrest, and inducing apoptosis. In vivo, the combination of radiation with PKI-587 significantly inhibited tumor growth. These findings suggest the usefulness of PKI-587 on radiosensitization of HCC cells by inhibiting the PI3K/AKT/mTOR and DNA damage repair pathways. The combination of ionizing radiation and PKI-587 may be a strategy to improve the efficacy of treating HCC.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCell ProliferationCell SurvivalChemoradiotherapyFemaleGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMiceMorpholinesPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRadiation-Sensitizing AgentsgedatolisibMorpholinesMTOR protein, humanPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRadiation-Sensitizing AgentsTOR Serine-Threonine KinasesTriazines

Identifiers

PMID34665844
PMCPMC8525768
OpenAlexW3206638464

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.