lusianthridin and Lung-Neoplasms

Cancer stem cells (CSCs) are well-recognized as a majority cause of treatment failure and can give rise to relapse. The discovery of compounds attenuating CSCs' properties is crucial for enabling advances in novel therapeutics to limit recurrence. CSCs' features in lung cancer are regulated through a reduction in Src-STAT3-c-Myc, which drives cancer progression, drug resistance, and metastasis.. The effect of lusianthridin suppresses CSC-like phenotypes was determined by 3D culture and anchorage independent growth. The expression of CSC markers and associated proteins were determined by Western blot analyses. Protein ubiquitination and degradation were assessed using immunoprecipitation.. Herein, we report that lusianthridin, a pure compound from Dendrobium venustum, dramatically suppressed CSCs in lung cancer cells as verified by several CSC phenotype assessments and CSC markers. The CSC phenotypes in lusianthridin-treated cells were suppressed through downregulation of Src-STAT3-c-Myc pathways. Ectopic Src introduced by the transfection augmented CSC phenotypes in lung cancer cells through STAT3 (increased active p-STAT3. These findings revealed a novel pharmacological action and the underlying mechanism of lusianthridin in negatively regulating CSC-like phenotypes and sensitizing resistant cancer cells to cemetery.

Topics: AC133 Antigen; Aldehyde Dehydrogenase 1 Family; Antineoplastic Agents, Phytogenic; ATP Binding Cassette Transporter, Subfamily G, Member 2; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cisplatin; Dasatinib; Down-Regulation; Humans; Lung Neoplasms; Neoplasm Proteins; Neoplastic Stem Cells; Phenanthrenes; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-myc; Retinal Dehydrogenase; Spheroids, Cellular; src-Family Kinases; STAT3 Transcription Factor