scholarly journals Resveratrol mediates cell cycle arrest and cell death in human esophageal squamous cell carcinoma by directly targeting the EGFR signaling pathway

2016 ◽  
Vol 13 (1) ◽  
pp. 347-355 ◽  
Author(s):  
Zixuan Jin ◽  
Wei Feng ◽  
Ying Ji ◽  
Longyu Jin
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Cell Death ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Cycle Arrest ◽  
Signaling Pathway ◽  
Egfr Signaling ◽  
Cycle Arrest ◽  
Egfr Signaling Pathway

scholarly journals α-Mangostin Induces Apoptosis and Cell Cycle Arrest in Oral Squamous Cell Carcinoma Cell

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Hyun-Ho Kwak ◽  
In-Ryoung Kim ◽  
Hye-Jin Kim ◽  
Bong-Soo Park ◽  
Su-Bin Yu
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Cell Death ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Cycle Arrest ◽  
Squamous Cell ◽  
G1 Phase ◽  
Cycle Arrest ◽  
Related Proteins

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.

Dehydrocostus Lactone Induces Apoptosis and Cell Cycle Arrest through Regulation of JAK2/STAT3/PLK1 Signaling Pathway in Human Esophageal Squamous Cell Carcinoma Cells

2021 ◽  
Vol 21 ◽  
Author(s):  
Ganghua Yang ◽  
Binwu Sheng ◽  
Ruixiang Li ◽  
Qinhong Xu ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Cycle Arrest ◽  
Apoptosis Induction ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
Dehydrocostus Lactone

Background: Dehydrocostus lactone (DEH), one of the sesquiterpene lactones, has shown extensive pharmaceutical activities, including anti-cancer activity. However, its effects on human esophageal squamous cell carcinoma (ESCC) cells still unknown. Objective: To investigate the effect of DEH on ESCC cells and the underling molecular mechanisms. Method: The cell proliferation was tested using CCK-8 and colony formation assay. Apoptosis was analyzed by flow cytometry, hoechst staining and caspase-3 activity assay. Cell cycle was analyzed by flow cytometry. IL-6 (STAT3 activator) was used to activate JAK2/STAT3 pathway. Immunofluorescence assay was performed to detect intracellular location of STAT3. SiRNA transfection was performed to knock down the expression of PLK1. The protein expression was analyzed by western blotting assay. Result: DHE treatment significantly reduced the viability of ESCC cells through apoptosis induction and cell cycle arrest. Furthermore, DHE treatment significantly inhibited the phosphorylation of JAK2 and STAT3. IF assay showed that distribution of STAT3 in nucleus was decreased by DHE treatment. In addition, coculture with IL-6 significantly prevented the inhibition of phosphorylation of JAK2 and STAT3 by DHE treatment, and partly reversed the effect of DHE on ESCC cells. Moreover, DHE treatment significantly down-regulated the expression of PLK1, which was partly reversed by IL-6 coculture. Finally, knock down of PLK1 using siRNA reduced the viability of ESCC cells and induced apoptosis and cell cycle arrest. Conclusion: our study demonstrated that DHE have potent anti-cancer effect on ESCC cells through apoptosis induction and cell cycle arrest via JAK2/STAT3/PLK signaling pathway.

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