ABSTRACT
OBJECTIVE: The aim of this study was to examine the antitumor effects of Qilan preparation on oral squamous cell carcinoma (OSCC) and to investigate its underlying mechanisms of action. METHODS: Cell proliferation, cell cycle distribution and apoptosis were examined using cell counting kit-8 (CCK8) and flow cytometry (FCM). The expression of PTEN and PDCD4 were determined by western blot. Changes in miR-21 levels were quantified using TaqMan stem-loop real-time PCR. After miR-21 was transiently transfected into Tca8113 cells using Lipofectamine®3000, cell proliferation, apoptosis and miR-21 and PDCD4 expression levels were measured. RESULTS: Qilan preparation inhibited Tca8113 cell growth in a dose- and time-dependent manner by inducing apoptosis and cell cycle arrest in S-phase, decreasing miR-21 levels and increasing PTEN and PDCD4 expression. MiR-21 overexpression reversed the Qilan preparation-induced suppression of cell proliferation and induction of apoptosis while also blocking the increase in PDCD4. CONCLUSIONS: Our study revealed, for the first time, the ability of Qilan preparation to suppress TSCC cell growth and elucidated that Qilan preparation elicits its anti-cancer actions either the miR-21/PDCD4 or PTEN pathway.
Subject(s)
Carcinoma, Squamous Cell , MicroRNAs , Mouth Neoplasms , Tongue Neoplasms , Apoptosis , Apoptosis Regulatory Proteins/genetics , Apoptosis Regulatory Proteins/metabolism , Apoptosis Regulatory Proteins/pharmacology , Carcinoma, Squamous Cell/drug therapy , Carcinoma, Squamous Cell/genetics , Carcinoma, Squamous Cell/metabolism , Cell Line, Tumor , Cell Proliferation , Gene Expression Regulation, Neoplastic , Humans , MicroRNAs/genetics , RNA-Binding Proteins/genetics , RNA-Binding Proteins/metabolism , RNA-Binding Proteins/pharmacology , Tongue/metabolism , Tongue/pathology , Tongue Neoplasms/drug therapy , Tongue Neoplasms/genetics , Tongue Neoplasms/metabolismABSTRACT
OBJECTIVE: To study the effect of Chinese herbal medicine 1023 Recipe in blocking cancer transformation of experimental oral precancerous lesion and its mechanism. METHODS: We treated the experimental oral precancerous lesion in hamster's cheek pouch using 1023 Recipe (consisting of Radix Astragali, Gynostemma Pentaphyllum, Rhizoma Chuanxiong and selenium-rich green tea) for 6 weeks, and observed its effect in blocking cancer transformation, detected 2 kinds of agglutinin receptors (receptors of wheat germ agglutinin and Ricinus communis agglutinin) in the mucosa of the hamster's cheek pouch. RESULTS: The rate of cancer transformation in 1023 Recipe treated group was lower than that in the control group without treatment (P<0.05). Agglutinin receptors in the two groups were different significantly. CONCLUSION: 1023 Recipe is effective in treating hyperplasia, and can prevent its cancer transformation. The mechanism may be that 1023 Recipe can induce precancerous lesions to differentiate into normal tissues.
