ArticleJournal of Cancer2018
The anti-tumor effects of dual PI3K/mTOR inhibitor BEZ235 and histone deacetylase inhibitor Trichostatin A on inducing autophagy in esophageal squamous cell carcinoma.
Article in Journal of Cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Design, synthesis, and biological evaluation of procaine-based triazole-isoxazoline hybrids as selective PI3K/mTOR inhibitors for esophageal cancer therapy:RSC medicinal chemistry · 2026Article
- Liraglutide improves depressive and cognitive deficits in a high-fat diet rat model of obesity: the role of hippocampal autophagy and the PI3K/Akt/mTOR pathway.Psychopharmacology · 2025Article
- PIK75 effectively reverses PI3K‒AKT activation caused by palbociclib resistance and synergistically inhibits the progression of esophageal squamous cell carcinoma.Scientific reports · 2025Article
- Restoration of Autophagy and Apoptosis in Myelodysplastic Syndromes: The Effect of Azacitidine in Disease Pathogenesis.Current issues in molecular biology · 2025Article
- IL-17A regulates airway remodelling in COPD through the PI3K/AKT/mTOR pathway.Scientific reports · 2025Article
- Gene Expression Analysis of Autophagy Markers in Primary and Secondary Myelofibrosis.Journal of clinical medicine · 2025Article
- Dual PI3K/mTOR inhibitor NVP-BEZ235 induces cell cycle arrest via autophagy mediated protein degradation of RPL19 in nephroblastoma cell.Frontiers in pharmacology · 2025Article
- miR-30c-5p inhibits esophageal squamous cell carcinoma progression by repressing the PI3K/AKT signaling pathway.Thoracic cancer · 2024Article
- Interleukin-1β/Interleukin (IL)-1-Receptor-Antagonist (IL1-RA) Axis in Invasive Bladder Cancer-An Exploratory Analysis of Clinical and Tumor Biological Significance.International journal of molecular sciences · 2024Article
- Review
- PDK1 inhibition reduces autophagy and cell senescence through the PI3K/AKT signalling pathway in a cigarette smoke mouse emphysema model.Experimental and therapeutic medicine · 2023Article
- Unraveling the Complexity of Regulated Cell Death in Esophageal Cancer: from Underlying Mechanisms to Targeted Therapeutics.International journal of biological sciences · 2023Review
- Pharmacological Properties of Trichostatin A, Focusing on the Anticancer Potential: A Comprehensive Review.Pharmaceuticals (Basel, Switzerland) · 2022Review
- A Review: PI3K/AKT/mTOR Signaling Pathway and Its Regulated Eukaryotic Translation Initiation Factors May Be a Potential Therapeutic Target in Esophageal Squamous Cell Carcinoma.Frontiers in oncology · 2022Review
- PI3K/Akt/mTOR Signaling Pathway: Role in Esophageal Squamous Cell Carcinoma, Regulatory Mechanisms and Opportunities for Targeted Therapy.Frontiers in oncology · 2022Review
- DHW-208, A Novel Phosphatidylinositol 3-Kinase (PI3K) Inhibitor, Has Anti-Hepatocellular Carcinoma Activity Through Promoting Apoptosis and Inhibiting Angiogenesis.Frontiers in oncology · 2022Article
- Targeting Autophagy with Natural Products as a Potential Therapeutic Approach for Cancer.International journal of molecular sciences · 2021Review
- Trichostatin A ameliorates Alzheimer's disease-related pathology and cognitive deficits by increasing albumin expression and Aβ clearance in APP/PS1 mice.Alzheimer's research & therapy · 2021Article
- The PI3K/AKT/mTOR pathway regulates autophagy to induce apoptosis of alveolar epithelial cells in chronic obstructive pulmonary disease caused by PM2.5 particulate matter.The Journal of international medical research · 2020Article
- Comprehensive Analysis of the Relationships Between Tumor Mutation Burden With Immune Infiltrates in Cervical Cell Carcinoma.Frontiers in molecular biosciences · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect and regulation of autophagy-related proteins Beclin-1 and LC3 in esophageal squamous cell carcinoma have not been fully studied. The aim of this study was to assess the expression of Beclin-1 and LC3 in ESCCs, and to investigate the association between the two markers and clinicopathological characteristics as well as prognosis. Meanwhile, we explored the anti-tumor effect of the PI3K/mTOR dual inhibitor BEZ235 and the histone deacetylase inhibitor TSA on inducing autophagy in ESCC cells. Our study included 118 ESCC tumors and paired non-tumor esophageal mucosa tissues. Beclin-1 and LC3 expression were performed by immunohistochemistry. Human ESCC cells Eca-109 and TE-1 were treated with BEZ235 and TSA either alone or in combination in Vitro. The expression of both Beclin-1 and LC3 proteins were decreased significantly in ESCCs, but there was no significant relation between the expression of Beclin-1 and LC3 (P = 0.427). The negative expression of either Beclin-1 or LC3 was associated with advanced TNM stages (P = 0.006 and P<0.001, respectively). Patients with a high expression of Beclin-1 and LC3 predict better prognosis. In Vitro co-treatment with BEZ235 and TSA showed a synergistic effect on inhibition of ESCC cell viability and induction of autophagy with the increasing expressions of Beclin-1, LC3-II and the ratio of LC3-II/LC3-I. Our results demonstrated that the autophagy-related proteins Beclin-1 and LC3 were decreased in ESCCs and the low expression of the two markers predicted a worse prognosis. The co-treatment of BEZ235 and TSA significantly induced autophagy and enhanced anti-tumor activities, provided a new effective therapeutic target in ESCCs.
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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.