Sclareol Inhibit Cell Growth and Induces Apoptosis via Activation of p53/p21 Signaling Pathways in Human Oral Squamous Cell Carcinoma Cells
Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine
ABSTRACT One of the most common prevalent forms of cancer in the world is oral squamous cell carcinoma (OSCC). In the present study, we explore the chemotherapeutic effect of Sclareol on human oral carcinoma KB cells in scientifically found that cellular and molecular alterations. The human oral carcinoma KB cell and African green monkey kidney normal cell line (Vero) were evaluated for a several types of investigations following they had been various concentrations of Sclareol (5–50 µM) and cisplatin (0–10 µM) for 24 h. Additionally, we exhibited that sclareol induces cytotoxicity effect by MTT assay, Reactive oxidative stress (ROS) was measured by DCFH‐DA staining assay, loss of mitochondrial membrane potential (Δψm) was assessed by Rho123 staining method, nuclear condensation, and apoptotic morphological changes was investigated by DAPI and AO/EtBr staining in KB cells. Sclareol promoted oxidative stress via an imbalance in redox status and increased DNA damage in human oral carcinoma KB cells. Besides, Sclareol induces apoptosis by activating dependent p21, thereby down‐regulating the expression levels of phosphorylation of Rb (ser 780), cyclin D1, and cyclin‐E. Furthermore, it is associated with mitochondrial‐mediated apoptotic and proapoptotic markers, as evidenced by the downregulated Bcl‐2 protein and the upregulation of (Bax, Cytochrome C, Cleaved PARP, Cleaved Caspase and Caspase‐9 &‐3) induced apoptosis signaling through p53 independent pathways. Therefore, our pre
Abstract
ABSTRACT One of the most common prevalent forms of cancer in the world is oral squamous cell carcinoma (OSCC). In the present study, we explore the chemotherapeutic effect of Sclareol on human oral carcinoma KB cells in scientifically found that cellular and molecular alterations. The human oral carcinoma KB cell and African green monkey kidney normal cell line (Vero) were evaluated for a several types of investigations following they had been various concentrations of Sclareol (5–50 µM) and cisplatin (0–10 µM) for 24 h. Additionally, we exhibited that sclareol induces cytotoxicity effect by MTT assay, Reactive oxidative stress (ROS) was measured by DCFH‐DA staining assay, loss of mitochondrial membrane potential (Δψm) was assessed by Rho123 staining method, nuclear condensation, and apoptotic morphological changes was investigated by DAPI and AO/EtBr staining in KB cells. Sclareol promoted oxidative stress via an imbalance in redox status and increased DNA damage in human oral carcinoma KB cells. Besides, Sclareol induces apoptosis by activating dependent p21, thereby down‐regulating the expression levels of phosphorylation of Rb (ser 780), cyclin D1, and cyclin‐E. Furthermore, it is associated with mitochondrial‐mediated apoptotic and proapoptotic markers, as evidenced by the downregulated Bcl‐2 protein and the upregulation of (Bax, Cytochrome C, Cleaved PARP, Cleaved Caspase and Caspase‐9 &‐3) induced apoptosis signaling through p53 independent pathways. Therefore, our present study findings suggest that Sclareol could be the productive new chemotherapeutic agent for against oral squamous cell carcinoma. The Schematic representation of the possible molecular mechanism of sclareol induces apoptosis through p53 and p21‐associated signaling in KB cells. graphical