Evidence map›Paper›PMID 33978839›Full record

ArticleCancer chemotherapy and pharmacology2021

Autophagy inhibitor potentiates the antitumor efficacy of apatinib in uterine sarcoma by stimulating PI3K/Akt/mTOR pathway.

Shucheng Chen, Lan Yao

Abstract read
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In one paragraph

Article in Cancer chemotherapy and pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  6. Sestrin2 in cancer: a foe or a friend?Biomarker research · 2022
    Review
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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

2 authors at 1 institution in 1 country.

Shucheng ChenDepartment of Gynecology, Fourth Hospital of Hebei Medical University, No.12, Jiankang Road, Shijiazhuang, 050011, Hebei, China.
Lan YaoDepartment of Gynecology, Fourth Hospital of Hebei Medical University, No.12, Jiankang Road, Shijiazhuang, 050011, Hebei, China. cradle20022001@yeah.net.ORCID 0000-0001-8639-0721
Hebei Medical University · CN

Funding

Hebei Provincial Department of Science and Technology 182777246
6 · The paper itself

Abstract

aimThe present study aims to examine the effects of apatinib combined with autophagy inhibitor 3-Methyladenine (3-MA) on the proliferation and apoptosis of human uterine sarcoma in FU-MMT-1 and MES-SA cells and its tumor inhibition effect in xenograft model of uterine sarcoma.

methodsDifferent concentrations of 3-MA and apatinib were used to treat the uterine sarcoma cell lines (MES-SA and FU-MMT-1 cells). The cell viability was detected by CCK8 method. Flow cytometry was used to detect the apoptosis and cell cycle. Wound closure assay and Transwell assay were performed to measure the migration ability of cells. Western blot was used to determine the apoptosis proteins and autophagy proteins. A nude mice sarcoma xenograft model was established and treated with apatinib alone, 3-MA alone, or combined incubation of them. Tumor size of xenograft and the mice survival rate were measured.

resultsCombination of 3-MA and apatinib significantly inhibited the proliferation and migration ability, but increased the apoptosis rate of uterine sarcoma cells compared to apatinib. The combination of 3-MA and apatinib significantly limited the tumor size of xenograft and increased the survival rate of mice compared to apatinib alone. Apatinib inhibited the PI3K/Akt/mTOR pathway, while 3-MA and the combination of 3-MA and apatinib significantly activated the PI3K/Akt/mTOR pathway and inhibited autophagy. Combination of 3-MA and apatinib increased apoptosis compared to apatinib alone. The expression of VEGFR-2 was not impacted by 3-MA.

conclusionCombination of apatinib and autophagy inhibitor 3-MA significantly inhibited the growth and migration of uterine sarcoma cells and xenograft. Autophagy inhibition may increase the antitumor effect of apatinib via the PI3K/Akt/mTOR pathway.

Indexed as

AnimalsAntineoplastic AgentsApoptosisAutophagyCell CycleCell Line, TumorCell ProliferationCell SurvivalFemaleHumansMiceMice, Inbred BALB CMice, NudePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyridinesAntineoplastic AgentsapatinibMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyridinesTOR Serine-Threonine Kinases3-MethyladenineApatinibApoptosisAutophagyUterine sarcoma

Identifiers

PMID33978839
OpenAlexW3163719935

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.