A marginal anticancer effect of regorafenib on pancreatic carcinoma cells in vitro, ex vivo, and in vivo

2017 ◽  
Vol 390 (11) ◽  
pp. 1125-1134 ◽  
Author(s):  
Barbara Mayer ◽  
Svetlana Karakhanova ◽  
Nathalie Bauer ◽  
Li Liu ◽  
Yifan Zhu ◽  
...  
Keyword(s):  
Pancreatic Carcinoma ◽  
Ex Vivo ◽  
Carcinoma Cells ◽  
Anticancer Effect

scholarly journals The ATP-Competitive mTOR Inhibitor INK128 Enhances In Vitro and In Vivo Radiosensitivity of Pancreatic Carcinoma Cells

2013 ◽  
Vol 20 (1) ◽  
pp. 110-119 ◽  
Author(s):  
Thomas J. Hayman ◽  
Amy Wahba ◽  
Barbara H. Rath ◽  
Heekyong Bae ◽  
Tamalee Kramp ◽  
...  
Keyword(s):  
Pancreatic Carcinoma ◽  
Mtor Inhibitor ◽  
Carcinoma Cells

scholarly journals Vitamin D receptors and anti-proliferative effects of vitamin D derivatives in human pancreatic carcinoma cells in vivo and in vitro

1997 ◽  
Vol 76 (8) ◽  
pp. 1017-1020 ◽  
Author(s):  
KW Colston ◽  
SY James ◽  
EA Ofori-Kuragu ◽  
L Binderup ◽  
AG Grant
Keyword(s):  
Vitamin D ◽  
Pancreatic Carcinoma ◽  
Carcinoma Cells ◽  
Vitamin D Receptors

scholarly journals Small interfering RNAs targeting mutant K-ras inhibit human pancreatic carcinoma cells growth in vitro and in vivo

2006 ◽  
Vol 5 (12) ◽  
pp. 1693-1698 ◽  
Author(s):  
Hong Zhu ◽  
Zhi Yong Liang ◽  
Xin Yu Ren ◽  
Tong Hua Li
Keyword(s):  
Pancreatic Carcinoma ◽  
Carcinoma Cells ◽  
Small Interfering Rnas

Adenovirus-mediated siRNA targeting Mcl-1 gene increases radiosensitivity of pancreatic carcinoma cells in vitro and in vivo

Surgery ◽  
2010 ◽  
Vol 147 (4) ◽  
pp. 553-561 ◽  
Author(s):  
Xiang Guoan ◽  
Wang Hanning ◽  
Chen Kaiyun ◽  
Liu Hao
Keyword(s):  
Pancreatic Carcinoma ◽  
Carcinoma Cells

Human pancreatic carcinoma cells are sensitive to photodynamic therapy in vitro and in vivo

1999 ◽  
Vol 86 (7) ◽  
pp. 899-906 ◽  
Author(s):  
A. Hajri ◽  
S. Coffy ◽  
F. Vallat ◽  
S. Evrard ◽  
J. Marescaux ◽  
...  
Keyword(s):  
Photodynamic Therapy ◽  
Pancreatic Carcinoma ◽  
Carcinoma Cells

scholarly journals Novel estradiol analogue induces apoptosis and autophagy in esophageal carcinoma cells

2014 ◽  
Vol 19 (1) ◽  
Author(s):  
Elize Wolmarans ◽  
Thandi Mqoco ◽  
Andre Stander ◽  
Sandra Nkandeu ◽  
Katherine Sippel ◽  
...  
Keyword(s):  
Cell Death ◽  
Esophageal Carcinoma ◽  
Ex Vivo ◽  
Apoptotic Cell ◽  
Critical Role ◽  
Carcinoma Cells ◽  
In Vivo Studies ◽  
Apoptotic Pathway

AbstractCancer is the second leading cause of death in South Africa. The critical role that microtubules play in cell division makes them an ideal target for the development of chemotherapeutic drugs that prevent the hyperproliferation of cancer cells. The new in silico-designed estradiol analogue 2-ethyl-3-O-sulfamoylestra-1,3,5(10)16-tetraene (ESE-16) was investigated in terms of its in vitro antiproliferative effects on the esophageal carcinoma SNO cell line at a concentration of 0.18 μM and an exposure time of 24 h. Polarization-optical differential interference contrast and triple fluorescent staining (propidium iodide, Hoechst 33342 and acridine orange) revealed a decrease in cell density, metaphase arrest, and the occurrence of apoptotic bodies in the ESE-16-treated cells when compared to relevant controls. Treated cells also showed an increase in the presence of acidic vacuoles and lysosomes, suggesting the occurrence of autophagic processes. Cell death via autophagy was confirmed using the Cyto-ID autophagy detection kit and the aggresome detection assay. Results showed an increase in autophagic vacuole and aggresome formation in ESE-16 treated cells, confirming the induction of cell death via autophagy. Cell cycle progression demonstrated an increase in the sub-G1 fraction (indicative of the presence of apoptosis). In addition, a reduction in mitochondrial membrane potential was also observed, which suggests the involvement of apoptotic cell death induced by ESE-16 via the intrinsic apoptotic pathway. In this study, it was demonstrated that ESE-16 induces cell death via both autophagy and apoptosis in esophageal carcinoma cells. This study paves the way for future investigation into the role of ESE-16 in ex vivo and in vivo studies as a possible anticancer agent.

Transient silencing of galectin-3 expression promotes both in vitro and in vivo drug-induced apoptosis of human pancreatic carcinoma cells

2011 ◽  
Vol 28 (4) ◽  
pp. 367-376 ◽  
Author(s):  
Tsutomu Kobayashi ◽  
Tatsuo Shimura ◽  
Toshiki Yajima ◽  
Norio Kubo ◽  
Kenichiro Araki ◽  
...  
Keyword(s):  
Pancreatic Carcinoma ◽  
Carcinoma Cells ◽  
Drug Induced ◽  
Galectin 3 ◽  
Induced Apoptosis

scholarly journals Silencing of decoy receptor 3 (DcR3) expression by siRNA in pancreatic carcinoma cells induces Fas ligand-mediated apoptosis in vitro and in vivo

2013 ◽  
Vol 32 (3) ◽  
pp. 653-660 ◽  
Author(s):  
JIAN ZHOU ◽  
SHIDUO SONG ◽  
SONGBIN HE ◽  
ZHENXIN WANG ◽  
BING ZHANG ◽  
...  
Keyword(s):  
Pancreatic Carcinoma ◽  
Fas Ligand ◽  
Carcinoma Cells ◽  
Decoy Receptor ◽  
Decoy Receptor 3

scholarly journals Enhanced Hsa-miR-181d/p-STAT3 and Hsa-miR-181d/p-STAT5A Ratios Mediate the Anticancer Effect of Garcinol in STAT3/5A-Addicted Glioblastoma

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1888 ◽  
Author(s):  
Heng-Wei Liu ◽  
Peter Mingjui Lee ◽  
Oluwaseun Adebayo Bamodu ◽  
Yu-Kai Su ◽  
Iat-Hang Fong ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Xenograft Model ◽  
Inverse Correlation ◽  
The Cancer Genome Atlas ◽  
Anticancer Effect ◽  
Garcinia Indica ◽  
Mouse Xenograft Model ◽  
Recurrent Gbm

Background: Glioblastoma (GBM), a malignant grade IV tumor, is the most malignant brain tumor due to its hyper-proliferative and apoptosis-evading characteristics. The signal transducer and activators of transcription (STAT) family genes, including STAT3 and STAT5A, have been indicated to play important roles in GBM progression. Increasing number of reports suggest that garcinol, a polyisoprenylated benzophenone and major bioactive component of Garcinia indica contains potent anti-cancer activities. Material and Methods: The present study investigated the anti-GBM effects of garcinol, focusing on the STAT3/STAT5A activation, using a combination of bioinformatics, in vitro, and ex vivo assays. Results: Our bioinformatics analysis of The Cancer Genome Atlas (TCGA)–GBM cohort (n = 173) showed that STAT3 and STAT5A are preferentially elevated in primary and recurrent GBM, compared to non-tumor brain tissues, and is significantly correlated with reduced overall survival. In support, our immunohistochemical staining of a GBM cohort (n = 45) showed an estimated 5.3-fold (p < 0.001) elevation in STAT3 and STAT5A protein expression in primary and recurrent GBM versus the non-tumor group. In vitro, garcinol treatment significantly suppressed the proliferative, invasive, and migratory potential of U87MG or GBM8401 cells, dose-dependently. In addition, garcinol anticancer effect significantly attenuated the GBM stem cell-like phenotypes, as reflected by diminished ability of U87MG or GBM8401 to form colonies and tumorspheres and suppressed expression of OCT4 and SOX2. Furthermore, analysis on GBM transcriptome revealed an inverse correlation between the level of STAT3/5A and hsa-miR-181d. Garcinol-mediated anti-GBM effects were associated with an increased hsa-miR-181d/STAT3 and hsa-miR-181d/5A ratio. The results were further verified in vivo using U87MG mouse xenograft model where administration of garcinol significantly inhibited tumor growth. Conclusions: We present evidence of anti-GBM efficacy of garcinol mediated by enhancing the hsa-miR-181d/STAT3 and hsa-miR-181d/5A ratios in GBM cells. Our findings suggest a potential new therapeutic agent for combating aggressive GBM.

Sign in / Sign up

Export Citation Format

Share Document