scholarly journals Cytotoxicity Effects ofAmoora rohitukaandchittagongaon Breast and Pancreatic Cancer Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Leo L. Chan ◽  
Sherine George ◽  
Irfan Ahmad ◽  
Saujanya L. Gosangari ◽  
Atiya Abbasi ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Alternative Medicine ◽  
Cancer Cells ◽  
Antibacterial Properties ◽  
Chemotherapeutic Agents ◽  
Normal Fibroblast ◽  
Label Free ◽  
Anticancer Properties ◽  
Pancreatic Cancer Cells ◽  
Mcf 7

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.

scholarly journals Knockdown of Snail Sensitizes Pancreatic Cancer Cells to Chemotherapeutic Agents and Irradiation

2010 ◽  
Vol 11 (12) ◽  
pp. 4891-4904 ◽  
Author(s):  
Kejun Zhang ◽  
Xuelong Jiao ◽  
Xiaoyi Liu ◽  
Bingyuan Zhang ◽  
Jigang Wang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Chemotherapeutic Agents ◽  
Pancreatic Cancer Cells

scholarly journals The Role of Mitochondria in the Chemoresistance of Pancreatic Cancer Cells

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 497
Author(s):  
Yibo Fu ◽  
Francesca Ricciardiello ◽  
Gang Yang ◽  
Jiangdong Qiu ◽  
Hua Huang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Mitochondrial Dynamics ◽  
Chemotherapeutic Agents ◽  
Aerobic Bacteria ◽  
Unresectable Pancreatic Cancer ◽  
First Line ◽  
Pancreatic Cancer Cells

The first-line chemotherapies for patients with unresectable pancreatic cancer (PC) are 5-fluorouracil (5-FU) and gemcitabine therapy. However, due to chemoresistance the prognosis of patients with PC has not been significantly improved. Mitochondria are essential organelles in eukaryotes that evolved from aerobic bacteria. In recent years, many studies have shown that mitochondria play important roles in tumorigenesis and may act as chemotherapeutic targets in PC. In addition, according to recent studies, mitochondria may play important roles in the chemoresistance of PC by affecting apoptosis, metabolism, mtDNA metabolism, and mitochondrial dynamics. Interfering with some of these factors in mitochondria may improve the sensitivity of PC cells to chemotherapeutic agents, such as gemcitabine, making mitochondria promising targets for overcoming chemoresistance in PC.

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

2014 ◽  
Author(s):  
Chandra K. Singh ◽  
Satwinderjeet Kaur ◽  
Jasmine George ◽  
Molly C. Pellitteri-Hahn ◽  
Cameron O. Scarlett ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Quantitative Proteomics ◽  
Label Free ◽  
Pancreatic Cancer Cells ◽  
Proteomics Approach

scholarly journals DNA damage induced by KP372-1 hyperactivates PARP1 and enhances lethality of pancreatic cancer cells with PARP inhibition

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Talysa Viera ◽  
Praveen L. Patidar
Keyword(s):  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Redox Cycling ◽  
Chemotherapeutic Agents ◽  
Parp Inhibition ◽  
Dna Breaks ◽  
Pancreatic Cancer Cells ◽  
Elevated Expression ◽  
Mechanistic Basis

AbstractThe overall prognosis for pancreatic cancer remains dismal and potent chemotherapeutic agents that selectively target this cancer are critically needed. Elevated expression of NAD(P)H:quinone oxidoreductase 1 (NQO1) is frequent in pancreatic cancer, and it offers promising tumor-selective targeting. Recently, KP372-1 was identified as a novel NQO1 redox cycling agent that induces cytotoxicity in cancer cells by creating redox imbalance; however, the mechanistic basis of KP372-1-induced cytotoxicity remains elusive. Here, we show that KP372-1 sensitizes NQO1-expressing pancreatic cancer cells and spares immortalized normal pancreatic duct cells, hTERT-HPNE. Notably, we found that KP372-1 is ~ 10- to 20-fold more potent than β-lapachone, another NQO1 substrate, against pancreatic cancer cells. Mechanistically, our data strongly suggest that reactive oxygen species produced by NQO1-dependent redox cycling of KP372-1 cause robust DNA damage, including DNA breaks. Furthermore, we found that KP372-1-induced DNA damage hyperactivates the central DNA damage sensor protein poly(ADP-ribose) polymerase 1 (PARP1) and activates caspase-3 to initiate cell death. Our data also show that the combination of KP372-1 with PARP inhibition creates enhanced cytotoxicity in pancreatic cancer cells. Collectively, our study provides mechanistic insights into the cytotoxicity instigated by KP372-1 and lays an essential foundation to establish it as a promising chemotherapeutic agent against cancer.

scholarly journals Gemcitabine Induces Microvesicle Particle Release in a Platelet-Activating Factor-Receptor-Dependent Manner via Modulation of the MAPK Pathway in Pancreatic Cancer Cells

2018 ◽  
Vol 20 (1) ◽  
pp. 32 ◽  
Author(s):  
Anita Thyagarajan ◽  
Sayali Kadam ◽  
Langni Liu ◽  
Lisa Kelly ◽  
Christine Rapp ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Mapk Pathway ◽  
Platelet Activating Factor ◽  
Chemotherapeutic Agents ◽  
Acid Sphingomyelinase ◽  
Mitogen Activated Protein Kinase ◽  
Human Pancreatic Cancer ◽  
Dependent Manner ◽  
Pancreatic Cancer Cells

Studies, including ours, have shown that pro-oxidative stressors, such as chemotherapeutic agents, generate oxidized lipids with agonistic platelet-activating factor (PAF) activity. Importantly, recent reports have implicated that these PAF-agonists are transported extracellularly via microvesicle particles (MVPs). While the role of PAF-receptor (PAF-R) has been implicated in mediating chemotherapy effects, its significance in chemotherapy-mediated MVP release in pancreatic cancer has not been studied. The current studies determined the functional significance of PAF-R in gemcitabine chemotherapy-mediated MVP release in human pancreatic cancer cells. Using PAF-R-expressing (PANC-1) and PAF-R-deficient (Hs766T) cells, we demonstrate that gemcitabine induces MVP release in a PAF-R-dependent manner. Blocking of PAF-R via PAF-R antagonist or inhibition of MVP generation via inhibitor of acid sphingomyelinase (aSMase) enzyme, significantly attenuated gemcitabine-mediated MVP release from PANC-1 cells, however, exerted no effects in Hs766T cells. Notably, MVPs from gemcitabine-treated PANC-1 cells, contained a measurable amount of PAF-agonists. Mechanistically, pretreatment with ERK1/2 or p38 inhibitors significantly abrogated gemcitabine-mediated MVP release, indicating the involvement of mitogen-activated protein kinase (MAPK) pathway in PAF-R-dependent gemcitabine-mediated MVP release. These findings demonstrate the significance of PAF-R in gemcitabine-mediated MVP release, as well as the rationale of evaluating PAF-R targeting agents with gemcitabine against pancreatic cancer.

scholarly journals Epithelial-to-Mesenchymal Transition in Pancreatic Adenocarcinoma

2010 ◽  
Vol 10 ◽  
pp. 1947-1957 ◽  
Author(s):  
Carla Cano ◽  
Yoshiharu Motoo ◽  
Juan L. Iovanna
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Epithelial To Mesenchymal Transition ◽  
Metastatic Potential ◽  
Chemotherapeutic Agents ◽  
Genetic Changes ◽  
Mesenchymal Transition ◽  
Pancreatic Cancer Cells ◽  
Microenvironmental Factors

Epithelial to mesenchymal transition (EMT) is a physiologic process that allows morphological and genetic changes of carcinoma cells from an epithelial to a mesenchymal phenotype, which is the basis of the high metastatic potential of pancreatic cancer cells. EMT is triggered by various tumor microenvironmental factors, including cytokines, growth factors, and chemotherapeutic agents. This review summarizes the state-of-the-art knowledge on the molecular mechanisms that support pancreatic cancer EMT and the evidences that support its involvement in invasiveness/aggressiveness, and the drug resistance of pancreatic cancer cells.

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