Resveratrol inhibits oral squamous cell carcinoma through induction of apoptosis and G2/M phase cell cycle arrest

Tumor Biology ◽  
2015 ◽  
Vol 37 (3) ◽  
pp. 2871-2877 ◽  
Author(s):  
Xiao-Dong Yu ◽  
Jing-lei Yang ◽  
Wan-Lin Zhang ◽  
Dong-Xu Liu
2013 ◽  
Vol 43 (5) ◽  
pp. 1675-1682 ◽  
Author(s):  
DANIELE MAGGIONI ◽  
WERNER GARAVELLO ◽  
ROBERTA RIGOLIO ◽  
LORENZO PIGNATARO ◽  
RENATO GAINI ◽  
...  

2012 ◽  
Vol 19 (1) ◽  
pp. 9 ◽  
Author(s):  
Ying-Ray Lee ◽  
Wei-Ching Wu ◽  
Wen-Tsai Ji ◽  
Jeff Chen ◽  
Ya-Ping Cheng ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Hyun-Ho Kwak ◽  
In-Ryoung Kim ◽  
Hye-Jin Kim ◽  
Bong-Soo Park ◽  
Su-Bin Yu

Mangosteen has long been used as a traditional medicine and is known to have antibacterial, antioxidant, and anticancer effects. Although the effects ofα-mangostin, a natural compound extracted from the pericarp of mangosteen, have been investigated in many studies, there is limited data on the effects of the compound in human oral squamous cell carcinoma (OSCC). In this study,α-mangostin was assessed as a potential anticancer agent against human OSCC cells.α-Mangostin inhibited cell proliferation and induced cell death in OSCC cells in a dose- and time-dependent manner with little to no effect on normal human PDLF cells.α-Mangostin treatment clearly showed apoptotic evidences such as nuclear fragmentation and accumulation of annexin V and PI-positive cells on OSCC cells.α-Mangostin treatment also caused the collapse of mitochondrial membrane potential and the translocation of cytochrome c from the mitochondria into the cytosol. The expressions of the mitochondria-related proteins were activated byα-mangostin. Treatment withα-mangostin also induced G1 phase arrest and downregulated cell cycle-related proteins (CDK/cyclin). Hence,α-mangostin specifically induces cell death and inhibits proliferation in OSCC cells via the intrinsic apoptosis pathway and cell cycle arrest at the G1 phase, suggesting thatα-mangostin may be an effective agent for the treatment of OSCC.


2015 ◽  
Vol 46 (6) ◽  
pp. 2606-2612 ◽  
Author(s):  
YOUNG-JOO JEON ◽  
WOONG BANG ◽  
JAE-CHEON SHIN ◽  
SEON-MIN PARK ◽  
JUNG-JAE CHO ◽  
...  

Life Sciences ◽  
2009 ◽  
Vol 85 (1-2) ◽  
pp. 26-32 ◽  
Author(s):  
Yu-Yi Hou ◽  
Mu-Ling Wu ◽  
Yu-Chun Hwang ◽  
Fang-Rong Chang ◽  
Yang-Chang Wu ◽  
...  

Oral Diseases ◽  
2021 ◽  
Author(s):  
Thi Thuy Tien Vo ◽  
Yinshen Wee ◽  
Hsin‐Chung Cheng ◽  
Ching‐Zong Wu ◽  
Yuh‐Lien Chen ◽  
...  

2021 ◽  
Author(s):  
Chuanning Wang ◽  
Zhiming Wang ◽  
Liping Zhang ◽  
Xiaoping Lin

Abstract Background: A large number of studies have shown that the imbalance of miRNA and its target genes can promote the development of tumors. The purpose of this study was to investigate the biological role and molecular mechanism of SERPINH1 and its upstream regulator miR-29c in oral squamous cell carcinoma (OSCC).Material and methods: The expression levels of SERPINH1 and miR-29c were detected by RT-qPCR and Western blotting. The proliferation, apoptosis, metastasis and cell cycle were detected by MTT assay, would healing assay, transwell assay, flow cytometry and dual luciferase reporter assay.Results: SERPINH1 is highly expressed in patients with OSCC and can be used as a prognostic biomarker for OSCC. Cell function experiments showed that silencing the expression of SERPINH1 inhibited the proliferation and migration of OSCC cells and caused cell cycle arrest at S phase. Bioinformatics analysis showed that there is a binding site between miR-29c and SERPINH1, indicating that miR-29c may regulate the expression of SERPINH1. In addition, miR-29c overexpression inhibited the proliferation and metastasis of OSCC cells, and subsequent rescue experiment showed that SERPINH1 overexpression can reverse the inhibitory effect of miR-29c in OSCC cell proliferation, migration, apoptosis and cell cycle arrest.Conclusions: MiR-29c can regulate the proliferation, migration, invasion and cell cycle of OSCC cells by targeting SERPINH1.


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