ArticleMolecular biotechnology2024
Inhibition of PI3K/Akt/mTOR Signaling Pathway Suppresses 5-Fluorouracil Resistance in Gastric Cancer.
Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 3 citations in OpenAlex.
- Agmatinase Facilitates Gastric Cancer Tumorigenesis Through PI3K/AKT-Mediated Enhancement of Proliferation, Invasion, and Stemness.Applied biochemistry and biotechnology · 2026Article
- The impact of the PI3K/AKT/mTOR signaling pathway on trastuzumab resistance in HER2-positive gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- The impact of the PI3K/AKT/mTOR signaling pathway on trastuzumab resistance in HER2-positive gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Potential roles of plant metabolites and Traditional Chinese Medicine formulas in regulating glycolysis-OXPHOS plasticity in gastric precancerous lesions and gastric cancer: a critical appraisal of the evidence.Frontiers in pharmacology · 2026Review
- miRNA-204-5p acts as a tumor suppressor in gastric cancer by inhibiting cell migration, invasion, and glycolysis via the RAB22A/PI3K/AKT axis.Scientific reports · 2025Article
- Prognostic Model Construction of Disulfidptosis-Related Genes and Targeted Anticancer Drug Research in Pancreatic Cancer.Molecular biotechnology · 2025Article
- TS-1 inhibits endometrial cancer cell proliferation, migration, and apoptosis by blocking the PI3K/AKT/mTOR signaling pathway.American journal of translational research · 2025Article
- Non-coding RNA in the Regulation of Gastric Cancer Tumorigenesis: Focus on microRNAs and Exosomal microRNAs.International journal of molecular and cellular medicine · 2024Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAt present, 5-Fluorouracil (5-FU) is a crucial anti-cancer drug and is widely used for the treatment of various carcinomas, including gastric cancer (GC). The resistance of GC cells to 5-FU is still a matter of great concern.
objectiveTo illustrate the role of PI3K/Akt/mTOR signaling in regulating the cell cycle progression and migration of 5-FU-resistant GC cells. MATERIAL AND
methodsAfter the establishment of drug-resistant GC cell lines, the effects of 5-FU and/or BEZ235 (the dual inhibitor of PI3K and mTOR) on the activity of parental or drug-resistant GC cells were explored. The viability and localization of GC cells (MKN-45 and MKN-74) and their drug-resistant cells (MKN-45/R and MKN-74/R) were assessed using MTT assays and immunofluorescence staining. The impacts of 5-FU and/or BEZ235 on GC cell cycle progression and cell migration were assessed via flow cytometry analyses and wound healing assays, respectively. GC tissues were collected from patients with GC sensitive or refractory to 5-FU chemotherapy. RT-qPCR and western blot were conducted to measure PI3K, AKT, and mTOR levels in GC cells or tissues.
resultsAfter 5-FU treatment, GC cells displayed 5-FU resistance and the viability of drug-resistant cells (MKN-45/R and MKN-74/R) was higher than that of parental cells (MKN-45 and MKN-74). The IC50 values for MKN-45 and MKN-45/R were 8.93 ug/ml and 140 ug/ml, and the values for MKN-74 and MKN-74/R were 3.93 ug/ml and 114.29 ug/ml. Additionally, the PI3K/Akt/mTOR signaling pathway was activated in drug-resistant GC cells and tumor tissues of patients refractory to 5-FU chemotherapy, as evidenced by high PI3K, Akt, and mTOR levels in MKN-45/R, MKN-74/R, and GC tissues resistant to 5-FU. BEZ235 promoted cell cycle arrest and suppressed the migration of GC cells. Moreover, the combination of BEZ235 and 5-FU led to more effective suppressive influence on cell cycle progression and cell migration relative to the single 5-FU or BEZ235 treatment.
conclusionsSilencing of the PI3K/Akt/mTOR signaling pathway suppressed the 5-FU resistance of GC cells.
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