ArticleMolecular medicine reports2020
Toosendanin induces apoptosis of MKN‑45 human gastric cancer cells partly through miR‑23a‑3p‑mediated downregulation of BCL2.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Toosendanin promotes prostate cancer cell apoptosis, ferroptosis and M1 polarization via USP39-mediated PLK1 deubiquitination.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- PLGA-based herb Toosendanin delivery system for efficient therapy of oral squamous cell carcinoma.BMC complementary medicine and therapies · 2025Article
- Antitumor effect of toosendanin on oral squamous cell carcinoma via suppression of p-STAT3.BMC oral health · 2023Article
- CTPS cytoophidia formation affects cell cycle progression and promotes TSN‑induced apoptosis of MKN45 cells.Molecular medicine reports · 2022Article
- [Interference of CTPS gene promotes toosendanin-induced apoptosis of human gastric cancer MKN-45 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Toosendanin, a late-stage autophagy inhibitor, sensitizes triple-negative breast cancer to irinotecan chemotherapy.Chinese medicine · 2022Article
- The therapeutic potential of natural products for treating pancreatic cancer.Frontiers in pharmacology · 2022Review
- MicroRNA-23a-3p influences the molecular mechanism of gastric cancer cells via CCL22/PI3K/Akt axis.Bioengineered · 2021Article
- Limonoids From the GenusFrontiers in pharmacology · 2021Review
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8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toosendanin (TSN) is a tetracyclic triterpenoid extracted from Melia toosendan Sieb, et Zucc, which primarily grows in specific areas of China. Although toosendanin (TSN) exerts antitumoral effects on various human cancer cells, its influence on gastric cancer (GC) is remains to be elucidated. MicroRNAs (miRNAs/miRs) serve crucial roles in apoptosis and proliferation of cancer cells. miR‑23a‑3p has been shown to be associated with human GC; however, the specific function of miR‑23a‑3p in GC remains unclear. Therefore, the present study aimed to elucidate the role of miR‑23a‑3p in the regulation of GC cell proliferation and apoptosis induced in vitro by TSN treatment. Subsequently, apoptosis‑related genes expression levels were quantified by reverse transcription‑quantitative PCR and western blot analysis, respectively, and the target relationship between miR‑23a‑3p and BCL2 was determined by luciferase reporter gene analysis. Additionally, cell proliferation and apoptosis experiments were carried out. The results indicated that TSN inhibited proliferation and induced apoptosis in MKN‑45 cells. Moreover, it upregulated the expression of miR‑23a‑3p. B‑cell lymphoma‑2 (BCL2) was identified as a potential target gene of miR‑23a‑3p, which was demonstrated to bind to the 3'‑untranslated region of BCL2 mRNA, as detected by the luciferase reporter assay. Further studies revealed that BCL2 expression was downregulated following overexpression of miR‑23a‑3p. In addition, the overexpression of the miR‑23a‑3p inhibited proliferation, induced G1 arrest and increased apoptosis in MKN‑45 cells. The results of the present study demonstrated that miR‑23a‑3p inhibited proliferation and induced apoptosis of GC cells, which may be attributable to its direct targeting of BCL2. These results may provide a novel insight into the apoptosis of GC cells, and may lead to investigations into the mechanisms of the effects of TSN.
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