cancer-therapy-and-biomarkers-2016

Volume 2, Issue 3(Suppl)

Oncol Cancer Case Rep

ISSN: 2471-8556 an open access journal

Page 51

Notes:

Cancer Therapy & Biomarkers 2016

December 05-07, 2016

conferenceseries

.com

CANCER THERAPY,

BIOMARKERS & CLINICAL RESEARCH

World Congress on

December 05-07, 2016 Philadelphia, USA

How many cell death pathways that

Doxorubicin

can affect HepG2 cells?

Noor Mohammed

University of Birmingham, UK

oxorubicin (DOX) is a potent antibiotic anti-cancer drug that is used either in isolation or in combination, for treating

ovary, haematological, breast, stomach, liver, and prostate cancers. This drug has the ability to damage DNA and inhibit

macromolecules (DNA and RNA) by producing free-radicals. Several studies have shown that Dox induces P53 activation

leading to apoptosis in both normal and tumour cells, by causing cytochrome c release from the mitochondria which ultimate-

ly leads to apoptosis via caspase 3. We have investigated the molecular mechanisms of DOX induced hepatic cell death. This

study shows that DOX can induce cell death in HepG2 cells through two different mechanisms. The use of caspase substrates

and caspase inhibitors confirm that apoptosis through caspase 9 and caspase 3 are involved. Using HepG2 cells transfected

with LC3-GFP, it was also noted that a high percentage of LC3-GFP punta were seen using fluorescence microscopy, following

DOX treatment, which suggests that autophagy is also involved. However, lactate dehydrogenase release assays and the use of

necrostatin, on DOX treated cells indicate that necrosis is unlikely to be involved.

Noor Mohammed, Oncol Cancer Case Rep 2016,2:3(Suppl)