Evidence map›Paper›PMID 31632530›Full record

ArticleAmerican journal of translational research2019

BEZ235 increases sorafenib inhibition of hepatocellular carcinoma cells by suppressing the PI3K/AKT/mTOR pathway.

Amin Li, Rongbo Zhang, Yinci Zhang, Xueke Liu, Ruikai Wang, Jiachang Liu, Xinkuang Liu, Yinghai Xie, Weiya Cao, Ruyue Xu and 5 more

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

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  8. c-Met up-regulates the expression of PD-L1 through MAPK/NF-κBp65 pathway.Journal of molecular medicine (Berlin, Germany) · 2022
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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

15 authors at 2 institutions in 1 country.

Amin LiMedical School, Anhui University of Science & Technology Huainan 232001, China.
Rongbo ZhangMedical School, Anhui University of Science & Technology Huainan 232001, China.
Yinci ZhangMedical School, Anhui University of Science & Technology Huainan 232001, China.
Xueke LiuMedical School, Anhui University of Science & Technology Huainan 232001, China.
Ruikai WangFirst Affiliated Hospital, Anhui University of Science & Technology Huainan 232001, China.
Jiachang LiuFirst Affiliated Hospital, Anhui University of Science & Technology Huainan 232001, China.
Xinkuang LiuFirst Affiliated Hospital, Anhui University of Science & Technology Huainan 232001, China.
Yinghai XieFirst Affiliated Hospital, Anhui University of Science & Technology Huainan 232001, China.
Weiya CaoMedical School, Anhui University of Science & Technology Huainan 232001, China.
Ruyue XuMedical School, Anhui University of Science & Technology Huainan 232001, China.
Yongfang MaMedical School, Anhui University of Science & Technology Huainan 232001, China.
Wenpeng CaiMedical School, Anhui University of Science & Technology Huainan 232001, China.
Binquan WuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Bengbu Medical College Bengbu 233004, China.
Shuyu CaiMedical School, Anhui University of Science & Technology Huainan 232001, China.
Xiaolong TangMedical School, Anhui University of Science & Technology Huainan 232001, China.
Anhui University of Science and Technology · CNFirst Affiliated Hospital of Bengbu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSorafenib is an oral multi-kinase inhibitor that inhibits hepatocellular carcinoma (HCC) via the Ras/Raf/MAPK pathway. However, sorafenib loses effectiveness because most tumors acquire drug resistance over time. As the PI3K/AKT/mTOR signaling pathway is also activated abnormally in HCC, we evaluated the effect of sorafenib, in combination with a dual PI3K/mTOR inhibitor, BEZ235, on HCC cell proliferation and survival in vitro. MATERIALS AND

methodsBiological phenotypes were analysed in HCC cell lines, parental and sorafenib-resistant HepG2 cells (HepG2 and HepG2

resultsBEZ235 enhanced sorafenib inhibition of cellular proliferation, migration, and promotion of apoptosis in HepG2 and HepG2

conclusionSorafenib/BEZ235 combination has potent anti-HCC cell activity. This anti-tumor activity is most likely multi-factorial, mainly involving PI3K down-regulation and AKT, mTOR and S6K dephosphorylation. Combined inhibition of PI3K/AKT/mTOR and Ras/Raf/MAPK pathways enhances sorafenib inhibition of HCC. The results of these in vitro studies suggest that trials of combined sorafenib and BEZ235 in the treatment of HCC should be considered.

Indexed as

BEZ235hepatocellular carcinomaHepG2 cellsPI3K/AKT/mTOR pathwaySorafenib

Identifiers

PMID31632530
PMCPMC6789287
OpenAlexW2989644126

What OpenQuestion holds

Textmetadata
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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.