Abstract 4533: Mechanism of anti-proliferative effects of sanguinarine in pancreatic cancer cells: A label-free quantitative proteomics approach

Author(s):  
Chandra K. Singh ◽  
Satwinderjeet Kaur ◽  
Jasmine George ◽  
Molly C. Pellitteri-Hahn ◽  
Cameron O. Scarlett ◽  
...  
Oncotarget ◽  
2015 ◽  
Vol 6 (12) ◽  
pp. 10335-10349 ◽  
Author(s):  
Chandra K. Singh ◽  
Satwinderjeet Kaur ◽  
Jasmine George ◽  
Minakshi Nihal ◽  
Molly C. Pellitteri Hahn ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Leo L. Chan ◽  
Sherine George ◽  
Irfan Ahmad ◽  
Saujanya L. Gosangari ◽  
Atiya Abbasi ◽  
...  

Chemotherapeutic agents for cancer are highly toxic to healthy tissues and hence alternative medicine avenues are widely researched. Majority of the recent studies on alternative medicine suggested thatAmoora rohitukapossesses considerable antitumor and antibacterial properties. In this work,rohitukaandchittagonga, fractionated with petroleum ether, dichloromethane, and ethanol, were explored for their anticancer potential against two breast cancer (MCF-7 and HTB-126) and three pancreatic cancer (Panc-1, Mia-Paca2, and Capan1). The human foreskin fibroblast, Hs68, was also included. Cytotoxicity of each extract was analyzed using the MTT assay and label-free photonic crystal biosensor assay. A concentration series of each extract was performed on the six cell lines. For MCF-7 cancer cells, thechittagonga(Pet-Ether and CH2Cl2) androhituka(Pet-Ether) extracts induced cytotoxicity; thechittagonga(EtoAC) androhituka(MeOH) extracts did not induce cytotoxicity. For HTB126, Panc-1, Mia-Paca2, and Capan-1 cancer cells, only thechittagongaCH2Cl2extract showed a significant cytotoxic effect. The extracts were not cytotoxic to normal fibroblast Hs68 cells, which may be correlated to the specificity ofAmooraextracts in targeting cancerous cells. Based on these results, further examination of the potential anticancer propertiesAmooraspecies and the identification of the active ingredients of these extracts is warranted.


2017 ◽  
Vol 89 (2) ◽  
pp. 1138-1146 ◽  
Author(s):  
Ling Hao ◽  
Jillian Johnson ◽  
Christopher B. Lietz ◽  
Amanda Buchberger ◽  
Dustin Frost ◽  
...  

2008 ◽  
Vol 7 (11) ◽  
pp. 2215-2228 ◽  
Author(s):  
Danmei Xu ◽  
Naoko Suenaga ◽  
Mariola J. Edelmann ◽  
Rafael Fridman ◽  
Ruth J. Muschel ◽  
...  

2020 ◽  
Author(s):  
Young Eun Kim ◽  
Eun-Kyung Kim ◽  
Min-Jeong Song ◽  
Tae-Young Kim ◽  
Ho Hee Jang ◽  
...  

AbstractOxaliplatin is a commonly used chemotherapeutic drug for the treatment of pancreatic cancer. Understanding the cellular mechanisms of oxaliplatin resistance is important for developing new strategies to overcome drug resistance in pancreatic cancer. In this study, we performed a stable isotope labelling by amino acids in cell culture (SILAC)-based quantitative proteomic analysis of oxaliplatin-resistant and sensitive pancreatic cancer PANC-1 cells. We identified 107 proteins whose expression levels changed between oxaliplatin-resistant and sensitive cells, which were involved in multiple biological processes, including DNA repair, drug response, apoptotic signalling, and the type 1 interferon signalling pathway. Notably, myristoylated alanine-rich C-kinase substrate (MARCKS) and wntless homolog protein (WLS) were upregulated in oxaliplatin-resistant cells compared to sensitive cells, as confirmed by qRT-PCR and Western blot analysis. We further demonstrated the activation of AKT and β-catenin signalling (downstream targets of MARCKS and WLS, respectively) in oxaliplatin-resistant PANC-1 cells. Additionally, we show that the siRNA-mediated suppression of both MARCKS and WLS enhanced oxaliplatin sensitivity in oxaliplatin-resistant PANC-1 cells. Taken together, our results provide insights into multiple mechanisms of oxaliplatin resistance in pancreatic cancer cells and reveal that MARCKS and WLS might be involved in the chemotherapeutic resistance in pancreatic cancer.


2009 ◽  
Vol 81 (2) ◽  
pp. 764-771 ◽  
Author(s):  
Yingchun Zhao ◽  
Wai-Nang Paul Lee ◽  
Shu Lim ◽  
Vay Liang Go ◽  
Jing Xiao ◽  
...  

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