jorunnamycin-a has been researched along with Lung-Neoplasms* in 3 studies
3 other study(ies) available for jorunnamycin-a and Lung-Neoplasms
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Target Identification of 22-(4-Pyridinecarbonyl) Jorunnamycin A, a Tetrahydroisoquinoline Derivative from the Sponge
A dysregulation of the cell-death mechanism contributes to poor prognosis in lung cancer. New potent chemotherapeutic agents targeting apoptosis-deregulating molecules have been discovered. In this study, 22-(4-pyridinecarbonyl) jorunnamycin A (22-(4'py)-JA), a synthetic derivative of bistetrahydroisoquinolinequinone from the Thai blue sponge, was semisynthesized by the Steglich esterification method, and its pharmacological mechanism in non-small-cell lung cancer (NSCLC) was elucidated by a network pharmacology approach. All predicted targets of 22-(4'py)-JA and genes related to NSCLC were retrieved from drug-target and gene databases. A total of 78 core targets were identified, and their associations were analyzed by STRING and Cytoscape. Gene ontology and KEGG pathway enrichment analyses revealed that molecules in mitogen-activated protein kinase (MAPK) signaling were potential targets of 22-(4'py)-JA in the induction of NSCLC apoptosis. In silico molecular docking analysis displayed a possible interaction of ERK1/2 and MEK1 with 22-(4'py)-JA. In vitro anticancer activity showed that 22-(4'py)-JA has strong cytotoxic and apoptosis-inducing effects in H460, H292 and A549 NSCLC cells. Furthermore, immunoblotting confirmed that 22-(4'py)-JA induced apoptotic cell death in an ERK/MEK/Bcl-2-dependent manner. The present study demonstrated that 22-(4'py)-JA exhibited a potent anticancer effect that could be further developed for clinical application and showed that network pharmacology approaches are a powerful tool to illustrate the molecular pathways of new drugs or compounds. Topics: Animals; Apoptosis; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Humans; Lung Neoplasms; Molecular Docking Simulation; Tetrahydroisoquinolines; Xestospongia | 2022 |
Jorunnamycin A Suppresses Stem-Like Phenotypes and Sensitizes Cisplatin-Induced Apoptosis in Cancer Stem-Like Cell-Enriched Spheroids of Human Lung Cancer Cells.
It has been recognized that cancer stem-like cells (CSCs) in tumor tissue crucially contribute to therapeutic failure, resulting in a high mortality rate in lung cancer patients. Due to their stem-like features of self-renewal and tumor formation, CSCs can lead to drug resistance and tumor recurrence. Herein, the suppressive effect of jorunnamycin A, a bistetrahydroisoquinolinequinone isolated from Thai blue sponge Topics: Animals; Apoptosis; Cell Line, Tumor; Cell Proliferation; Cell Survival; Cisplatin; Down-Regulation; Drug Synergism; Humans; Isoquinolines; Lung Neoplasms; Nanog Homeobox Protein; Neoplastic Stem Cells; Octamer Transcription Factor-3; Proto-Oncogene Proteins c-bcl-2; Quinolones; SOXB1 Transcription Factors; Spheroids, Cellular; Transcription Factors; Tumor Suppressor Protein p53; Xestospongia | 2021 |
Jorunnamycin A from
Metastasis is a key driving force behind the high mortality rate associated with lung cancer. Herein, we report the first study revealing the antimetastasis activity of jorunnamycin A, a bistetrahydroisoquinolinequinone isolated from a Thai blue sponge Topics: Animals; Anoikis; Cell Division; Cell Line, Tumor; Down-Regulation; Epithelial-Mesenchymal Transition; Humans; Isoquinolines; Lung Neoplasms; Proto-Oncogene Proteins c-bcl-2; Quinolones; Xestospongia | 2019 |