scholarly journals Tumor‐derived exosomes influence the cell cycle and cell migration of human esophageal cancer cell lines

2020 ◽  
Vol 111 (12) ◽  
pp. 4348-4358
Author(s):  
Yasunori Matsumoto ◽  
Masayuki Kano ◽  
Kentaro Murakami ◽  
Takeshi Toyozumi ◽  
Hiroshi Suito ◽  
...  
2019 ◽  
Vol 3 (s1) ◽  
pp. 5-5
Author(s):  
Randi Ryan ◽  
Shrikant Anant ◽  
Prabhu Ramamoorthy ◽  
Dharmalingam Subramaniam ◽  
Scott Weir

OBJECTIVES/SPECIFIC AIMS: Drug repositioning has the potential to accelerate translation of novel cancer chemotherapeutics from bench to bedside. The goal of this study was to determine the effects of ciclopirox olamine (CPX) on esophageal tumor cells. METHODS/STUDY POPULATION: We tested the effect of CPX on four esophageal cancer cell lines, assessing cell proliferation and viability by hexosaminidase and clonogenicity assay, respectively. We analyzed the effects of CPX on three-dimensional (3D) esophageal tumor cell spheroids. We also analyzed effects on cell cycle by flow cytometry. For mechanism, we performed western blots for proteins involved in cell cycle regulation, apoptosis and the Wnt/β-catenin pathway. For in vivo effects, we performed a murine xenograft model with intraperitoneal administration of CPX (100 mg/Kg body weight daily). RESULTS/ANTICIPATED RESULTS: CPX inhibited growth of all cell lines in a time and concentration-dependent manner. CPX also inhibited growth of esophageal spheroids. Cell cycle analysis demonstrated G0/G1 arrest in cells treated with CPX. Western blot analyses demonstrated decreased expression of cyclinD1, CDK4, CDK6, and transcriptionally active β-catenin, supporting the role of CPX in cell cycle inhibition and decreased β-catenin activity. Finally, treatment of nude mice with CPX significantly decreased tumor xenograft volume. DISCUSSION/SIGNIFICANCE OF IMPACT: CPX demonstrates anti-tumor properties in esophageal cancer cell lines. The current results justify further research into the mechanism of this inhibition. Additionally, given its established safety in humans, CPX is a potential candidate for repositioning as an adjunct treatment for esophageal cancer.


1996 ◽  
Vol 16 (12) ◽  
pp. 1001-1006 ◽  
Author(s):  
MASAAKI OKA ◽  
NORIO IIZUKA ◽  
KOHTARO YAMAMOTO ◽  
TOSHIKAZU GONDO ◽  
TOSHIHIRO ABE ◽  
...  

2010 ◽  
Vol 285 (11) ◽  
pp. 7986-7994 ◽  
Author(s):  
Yanyan Tian ◽  
Aiping Luo ◽  
Yiran Cai ◽  
Qin Su ◽  
Fang Ding ◽  
...  

2019 ◽  
Vol 18 ◽  
pp. 153303381984254
Author(s):  
Nannan Ao ◽  
Yingchu Dai ◽  
Qianping Chen ◽  
Yang Feng ◽  
Jingping Yu ◽  
...  

Objectives: Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential target pathways. Methods: Two human esophageal cancer cell lines, TE-1 and KYSE-150, were used in this study. Cell viability, cell cycle distribution, and apoptosis after Bortezomib treatment was detected by Cell Counting Kit-8, flow cytometry, and Annexin V/propidium iodide staining, respectively. The genes targeted by Bortezomib were analyzed at the messenger RNA level by microarray chips and quantitative real-time polymerase chain reaction. Results: The proliferation of human esophageal cancer cell lines was inhibited by Bortezomib in a dose- and time-dependent manner. Bortezomib treatment led to G2/M arrest and apoptosis. Microarray chips revealed multiple signaling pathways targeted by Bortezomib, including proteasome, endoplasmic reticulum, Wnt-, and calcium-mediated pathway. The expression patterns of 4 representative genes UBD, CUL3, HDAC6, and GADD45A were verified by quantitative real-time polymerase chain reaction and showed consistency with the microarray assay. Conclusion: Bortezomib could suppress cell viability, cause G2/M arrest, and induce apoptosis in human esophageal cancer cells, with possible targets including UBD, CUL3, HDAC6, and GADD45A.


2002 ◽  
Vol 53 (5) ◽  
pp. 417-429
Author(s):  
Masaru Sawataishi ◽  
Kenichi Takaya ◽  
Michio Kimura ◽  
Toshiko Yoshida ◽  
Kenichi Tazawa ◽  
...  

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