ArticleInternational journal of oncology2020
Effects of evodiamine on PI3K/Akt and MAPK/ERK signaling pathways in pancreatic cancer cells.
Article in International journal of oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Antitumor Effects of Evodiamine in Mice Model Experiments: A Systematic Review and Meta-Analysis.Frontiers in oncology · 2021Pooled it
- Bioactive plant and fungal metabolites in oral cancer: molecular mechanisms and translational potential.Frontiers in pharmacology · 2026Review
- Therapeutical potential of natural products in treatment of pancreatic cancer: a review.Molecular biology reports · 2025Review
- The impact of evodiamine on human anaplastic thyroid cancer therapy-anInternational journal of medical sciences · 2025Article
- Evodiamine inhibits proliferation and induces apoptosis of nasopharyngeal carcinoma cells via the SRC/ERBB2-mediated MAPK/ERK signaling pathway.Journal of translational medicine · 2024Article
- Evodiamine potentiates cisplatin-induced cell death and overcomes cisplatin resistance in non-small-cell lung cancer by targeting SOX9-β-catenin axis.Molecular biology reports · 2024Article
- Exploiting Nanotechnology for Drug Delivery: Advancing the Anti-Cancer Effects of Autophagy-Modulating Compounds in Traditional Chinese Medicine.International journal of nanomedicine · 2024Review
- Consistent RNA expression and RNA modification patterns in cardiotoxicity induced by Matrine and Evodiamine.Frontiers in pharmacology · 2024Article
- Evodiamine exerts anti-cancer activity including growth inhibition, cell cycle arrest, and apoptosis induction in human follicular thyroid cancers.American journal of cancer research · 2024Article
- Evodiamine: A Extremely Potential Drug Development Candidate of Alkaloids fromInternational journal of nanomedicine · 2024Review
- Carcinogenic Role and Clinical Significance of Histone H3-H4 Chaperone Anti-silencing Function 1 B (ASF1B) in Lung Adenocarcinoma.Journal of Cancer · 2024Article
- Research Progress of Indole Alkaloids: Targeting MAP Kinase Signaling Pathways in Cancer Treatment.Cancers · 2023Review
- Dietary Evodiamine Inhibits Atherosclerosis-Associated Changes in Vascular Smooth Muscle Cells.International journal of molecular sciences · 2023Article
- Traditional Chinese medicine Euodiae Fructus: botany, traditional use, phytochemistry, pharmacology, toxicity and quality control.Natural products and bioprospecting · 2023Review
- Evodiamine as an anticancer agent: a comprehensive review on its therapeutic application, pharmacokinetic, toxicity, and metabolism in various cancers.Cell biology and toxicology · 2023Review
- Effect of Evodiamine on Collagen-Induced Platelet Activation and Thrombosis.BioMed research international · 2022Article
- Evodiamine as the Active Compound of Evodiae fructus to Inhibit Proliferation and Migration of Prostate Cancer through PI3K/AKT/NF-Disease markers · 2022Article
- Article
- Research progress on evodiamine, a bioactive alkaloid ofExperimental and therapeutic medicine · 2021Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effective antitumor drug evodiamine (EVO) is attracting increased attention. Therefore, the present study aimed to investigate the effects of EVO on the proliferation, apoptosis and autophagy of human pancreatic cancer (PC) cell lines in vitro and in vivo. Human PANC‑1 and SW1990 PC cell lines were treated with different concentrations of EVO and proliferation was detected using a Cell Counting Kit (CCK)‑8 assay. Colony formation and wound‑healing assays showed that EVO inhibited PC cell viability and migration, and apoptosis was detected using flow cytometry. Western blotting and immunofluorescence detected the expression of proteins in PANC‑1 and SW1990 cells. The PANC‑1 cells were used to establish an orthotopic pancreatic tumor model in nude mice. Tumor‑bearing nude mice were administered with different concentrations of EVO, and growth was monitored. High‑resolution positron emission tomography and fluorine‑18‑labeled fluorodeoxyglucose were used to monitor the tumor/non‑tumor (T/NT) ratio and standard uptake value (SUV) of the mice, which were subsequently sacrificed to measure the transplanted tumor weight. Apoptosis increased with increasing EVO concentration. The EVO‑treated PC cells exhibited significantly higher expression of LC3II than the controls cells. EVO decreased LC3II, enhanced P62 and inhibited the expression of Akt, extracellular‑signal‑regulated protein kinase (ERK)1/2 and p38. Compared with the control group, the T/NT ratio, SUV and tumor weight decreased more markedly in the EVO‑treated group. The tumor expression of phosphorylated AKT, detected using immunohistochemistry, decreased with increasing EVO doses in vivo. EVO induced PC cell apoptosis by inhibiting phosphoinositide 3‑kinase/AKT and mitogen‑activated protein kinase/ERK and inhibiting the phosphorylation of signal transducer and activator of transcription activator 3 in PC cells to inhibit autophagy, suggesting that EVO may be considered as a novel PC treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.