1. Furowanin A-induced autophagy alleviates apoptosis and promotes cell cycle arrest via inactivation STAT3/Mcl-1 axis in colorectal cancer
- Author
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Junbao Gu, Xuebin Bao, and Zhao Ma
- Subjects
Male ,STAT3 Transcription Factor ,Cell cycle checkpoint ,Cell ,Mice, Nude ,Apoptosis ,General Biochemistry, Genetics and Molecular Biology ,Mice ,Autophagy ,Biomarkers, Tumor ,Tumor Cells, Cultured ,medicine ,Animals ,Humans ,General Pharmacology, Toxicology and Pharmaceutics ,STAT3 ,Cell Proliferation ,Mice, Inbred BALB C ,TUNEL assay ,integumentary system ,biology ,Chemistry ,Cell Cycle Checkpoints ,General Medicine ,Cell cycle ,Isoflavones ,Xenograft Model Antitumor Assays ,Gene Expression Regulation, Neoplastic ,Blot ,medicine.anatomical_structure ,biology.protein ,Cancer research ,Myeloid Cell Leukemia Sequence 1 Protein ,Colorectal Neoplasms - Abstract
Aim Furowanin A (Fur A) is a flavonoid isolated from Millettia pachycarpa Benth. Studies show its potent anti-neoplastic effects against leukemia cells. The aim of the present study was to determine the potential therapeutic effect of Fur A against colorectal cancer (CRC), and elucidate the underlying mechanism. Material and methods Cell Counting Kit-8 (CCK-8) assay was used to determine cell, and TUNEL and Annexin-V/PI staining was used to detect apoptosis and the cell cycle distribution. The expression levels of specific proteins in the CRC cells were analyzed by Western blotting. A xenograft model was also established to evaluate the therapeutic effect of Fur A in vivo. Key findings Fur A suppressed proliferation, blocked cell cycle progression, induced apoptosis and promoted autophagy in CRC cells. Interestingly, Fur A-induced autophagy functioned not only as a survival mechanism against apoptosis but also intensified the cell cycle arrest in CRC cells. In addition, Fur A mediated its effects via the inactivation of the STAT3/Mcl-1 axis. Significance Fur A is a promising drug candidate for the treatment and prevention of CRC.
- Published
- 2019
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