ArticleWorld journal of surgical oncology2021
Cyanidin-3-glucoside suppresses the progression of lung adenocarcinoma by downregulating TP53I3 and inhibiting PI3K/AKT/mTOR pathway.
Article in World journal of surgical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- A review of PI3K/AKT/mTOR inhibitors from traditional Chinese medicine: potential and perspective for activated phosphoinositide 3-kinase δ syndrome.Orphanet journal of rare diseases · 2026Review
- Systematic Investigation of Tumor Immune Microenvironment Modulation byPharmaceuticals (Basel, Switzerland) · 2026Article
- A TP53-Pathway-Based Prognostic Signature for Radiotherapy and Functional Validation of TP53I3 in Non-Small-Cell Lung Cancer.Cancers · 2026Article
- Anticancer Mechanisms of Bioactive Compounds from Sweet Potato (Foods (Basel, Switzerland) · 2025Review
- Anthocyanins: From Natural Colorants to Potent Anticancer Agents.Food science & nutrition · 2025Review
- Mechanisms of Ferroptosis-Related Genes in Gallbladder Cancer Based on Bioinformatics Analysis.Molecular biotechnology · 2025Article
- Critical Review on Anti-Obesity Effects of Anthocyanins Through PI3K/Akt Signaling Pathways.Nutrients · 2025Review
- Exposure to deltamethrin leads to gill liver damage, oxidative stress, inflammation, and metabolic disorders of Japanese flounder (Frontiers in toxicology · 2025Article
- Article
- The Potential of Crude and Partially Purified Black Rice Bran Extracts Obtained by Ultrasound-Assisted Extraction: Anti-Glycemic, Cytotoxicity, Cytoprotective, and Antitumoral Effects.Foods (Basel, Switzerland) · 2024Article
- Tumor-suppressive action of miR-30a-5p in lung adenocarcinoma correlates with ABL2 inhibition and PI3K/AKT pathway inactivation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Article
- Anthocyanins prevent the development and progression of urethane-induced lung cancer by regulating energy metabolism in mice.Food & nutrition research · 2024Article
- Integrating molecular, biochemical, and immunohistochemical features as predictors of hepatocellular carcinoma drug response using machine-learning algorithms.Frontiers in molecular biosciences · 2024Article
- Pan-cancer landscape of CENPO and its underlying mechanism in LUAD.Respiratory research · 2023Article
- Behind the Scenes of Anthocyanins-From the Health Benefits to Potential Applications in Food, Pharmaceutical and Cosmetic Fields.Nutrients · 2022Review
- Insights into the Mechanisms of Action of Proanthocyanidins and Anthocyanins in the Treatment of Nicotine-Induced Non-Small Cell Lung Cancer.International journal of molecular sciences · 2022Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe aim of this study is to unravel the role of Cyanidin-3-glucoside (C3G) and its potential mechanisms in lung adenocarcinoma (LUAD).
methodsThe cell clones, proliferation, apoptosis, migration, and invasion in H1299 and A549 cells were determined by colony formation assay, 5-ethynyl-20 deoxyuridine (EdU) assay, flow cytometry, and transwell assay, respectively. The expression of p53-induced gene 3 (TP53I3) was assessed and the prognostic values of TP53I3 in LUAD via the dataset from the Cancer Genome Atlas (TCGA). In addition, the mRNA and protein expressions were detected by quantitative real-time PCR (qRT-PCR) and western blot.
resultsC3G inhibited the proliferation, migration, and invasion of, and also promoted the apoptosis in H1299 and A549 cells. The database of TCGA showed TP53I3 was highly expressed in LUAD tissues and correlated with the poor prognosis of LUAD patients. Moreover, we also found that C3G inhibited the proliferation, migration and invasion, and promoted apoptosis in H1299 and A549 cells by downregulating TP53I3. Additionally, C3G could inhibit the activation of phosphatidylinositol 3'-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in H1299 and A549 cells by downregulating TP53I3.
conclusionThis study demonstrated that C3G could inhibit the proliferation, migration and invasion, and also facilitate the apoptosis through downregulating TP53I3 and inhibiting PI3K/AKT/mTOR pathway in LUAD.
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