piplartine and Carcinoma--Squamous-Cell

piplartine has been researched along with Carcinoma--Squamous-Cell* in 2 studies

Other Studies

2 other study(ies) available for piplartine and Carcinoma--Squamous-Cell

ArticleYear
Piperlongumine and p53-reactivator APR-246 selectively induce cell death in HNSCC by targeting GSTP1.
    Oncogene, 2018, Volume: 37, Issue:25

    Topics: Animals; Apoptosis; Biomarkers, Tumor; Carcinoma, Squamous Cell; Case-Control Studies; Cell Proliferation; Dioxolanes; Drug Therapy, Combination; Female; Follow-Up Studies; Gene Expression Regulation, Neoplastic; Glutathione S-Transferase pi; Head and Neck Neoplasms; Humans; Male; Mice; Mice, SCID; Prognosis; Quinuclidines; Tumor Cells, Cultured; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assays

2018
Piperlongumine Suppresses Proliferation of Human Oral Squamous Cell Carcinoma through Cell Cycle Arrest, Apoptosis and Senescence.
    International journal of molecular sciences, 2016, Apr-23, Volume: 17, Issue:4

    Oral squamous cell carcinoma (OSCC), an aggressive cancer originating in the oral cavity, is one of the leading causes of cancer deaths in males worldwide. This study investigated the antitumor activity and mechanisms of piperlongumine (PL), a natural compound isolated from Piper longum L., in human OSCC cells. The effects of PL on cell proliferation, the cell cycle, apoptosis, senescence and reactive oxygen species (ROS) levels in human OSCC cells were investigated. PL effectively inhibited cell growth, caused cell cycle arrest and induced apoptosis and senescence in OSCC cells. Moreover, PL-mediated anti-human OSCC behavior was inhibited by an ROS scavenger N-acetyl-l-cysteine (NAC) treatment, suggesting that regulation of ROS was involved in the mechanism of the anticancer activity of PL. These findings suggest that PL suppresses tumor growth by regulating the cell cycle and inducing apoptosis and senescence and is a potential chemotherapy agent for human OSCC cells.

    Topics: Acetylcysteine; Antineoplastic Agents; Apoptosis; Carcinoma, Squamous Cell; Caspase 3; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Proliferation; Cellular Senescence; Cyclin-Dependent Kinase Inhibitor p21; Dioxolanes; DNA Fragmentation; Humans; Mouth Neoplasms; Reactive Oxygen Species

2016