Evidence map›Paper›PMID 36547690›Full record

ArticleJournal of cancer research and clinical oncology2023

The antitumor effect of the novel agent MCL/ACT001 in pancreatic ductal adenocarcinoma.

Juan Yang, Yin Li, Xiao Han, Xiaolin Pei, Zhoujun Lin, Chenggang Li

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 27% 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, 7 citations in OpenAlex.

  1. Article
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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

6 authors at 1 institution in 1 country.

Juan YangState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No.38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China.
Yin LiState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No.38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China.
Xiao HanState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No.38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China.
Xiaolin PeiState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No.38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China.
Zhoujun LinState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No.38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China.
Chenggang LiState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No.38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China. lichenggang@nankai.edu.cn.ORCID http://orcid.org/0000-0002-5551-6093
Nankai University · CN

Funding

Fundamental Research Funds for the Central Universities Nankai University, #ZB19100128
6 · The paper itself

Abstract

purposePancreatic ductal adenocarcinoma (PDAC) is a major challenge in cancer therapy, there are more than four hundred thousand deaths per year, and the 5-year survival rate is less than 10%. The incidence continues to rise. Treatment with classic drugs offers limited therapeutic benefits. The aim of this study was to investigate the mechanism and effect of the new agent ACT001, the active metabolite of Micheliolide (MCL), in vitro and in vivo against PDAC.

methodsMTT assay, wound healing assay, and flow cytometry were used to assess the effects of MCL/ACT001 in vitro. DCFH-DA assay was used to assess ROS accumulation. Western blotting, immunohistochemical staining and TUNEL assay were also conducted to determine the mechanisms. PANC-1-Luc cells and bioluminescent reporter imaging were used to assess antitumor effect of ACT001 using a orthotopic xenograft model in vivo.

resultsMCL/ACT001 significantly inhibited cell growth in PDAC in a dose-dependent manner, induced cell apoptosis, cell migration and reactive oxygen species (ROS) accumulation in vitro. In vivo, ACT001 (400 mg/kg/day) inhibited PDAC tumor growth in orthotopic xenograft mice. We verified that EGFR and Akt were markedly overexpressed in PDAC cells and patient tumors. Mechanistic investigations revealed that MCL exerted its antitumor activity via regulation of the EGFR-Akt-Bim signaling pathway, thus inducing Bim expression both in vitro and in vivo.

conclusionMCL/ACT001 is a highly promising agent in the treatment of PDAC patients.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsAnimalsApoptosisCell Line, TumorCell ProliferationErbB ReceptorsFuransHumansMiceProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSesquiterpenes, GuaianeXenograft Model Antitumor AssaysACT001ErbB ReceptorsFuransmicheliolideProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSesquiterpenes, GuaianeAktApoptosisBimEGFRMCL/ACT001Pancreatic ductal adenocarcinoma (PDAC)

Identifiers

PMID36547690
PMCPMC11797479
OpenAlexW4312094491

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.