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Journal of Gastrointestinal & Digestive System | ISSN: 2161-069X | Volume: 8
&
&
October 29-30, 2018 | San Francisco, USA
International Conference on
Gastrointestinal Cancer and Therapeutics
4
th
World Congress on
Digestive & Metabolic Diseases
26
th
Annual Congress on
Cancer Science and Targeted Therapies
Actinonin represses TRAP1-key molecule to counter resistance in non small cell lung cancer
Priyanca Ahlawat
Post Graduate Institute of Medical Education and Research, India
Statement of the problem:
Lung cancer is the most widely prevalent type of cancer worldwide. Approximately 85% of such
cases are of non-small cell lung carcinoma histology. The emergence of resistance against prescribed chemotherapy has posed
additional trouble. Mitochondria play a critical role in themaintenance of cancer cell homeostasis. Researchers are now focusing
on understanding the importance of this organelle in cancer progression and designing novel therapeutics against it. More
than a decade ago, Actinonin, a peptidomimetic compound naturally produced by actinomycetes that inhibits human peptide
deformylase was observed to have anti-cancerous properties. It has been shown to disrupt the mitochondrial permeability
and compromise the cellular health via induction of apoptosis. On the other hand TRAP1, a cytoprotective mitochondrial
chaperone has proven to be involved in poor prognosis of resistant cases. However, the effect of actinonin on the expression of
TRAP1 has not been studied which might hold the key for apoptosis induction by actinonin.
Methodology &Theoretical Orientation:
The IC
50
of actinonin for non-small cell lung carcinoma cell line H520 was calculated
using MTT assay after 24hours of actinonin’s treatment. The IC
50
dose was used to treat the cells and mRNA expression was
analyzed for TRAP1, Caspase 8, HIF-1α, Vimentin, and N-Cadherin by real-time PCR. The apoptosis in H520 cells at 24hours
of actinonin treatment was analyzed using AnnexinV/PI staining.
Findings:
The mRNA expression at 24 hours exposure of H520 cells to actinonin, induced nearly four fold downregulation of
TRAP1 expression and a two-fold decrease in Caspase 8 expression. AnnexinV/PI staining confirmed cells in early and late
apoptosis with no necrosis upon 24 hours actinonin treatment.
Conclusion & Significance:
This study supports that actinonin can be utilized against lung cancer cases and other cancer types
in which
TRAP1
gene’s higher expression causes resistance against prescribed chemotherapy.
Biography
Priyanca Ahlawat is a research student in the Post Graduate Institute of Medical Education and Research, Chandigarh, India. Her research interests includes
molecular biology and mitochondrial biology of non small cell lung cancer and nanotechnology based delivery systems against cancer.
priyanca.91@gmail.comPriyanca Ahlawat, J Gastrointest Dig Syst 2018, Volume 8
DOI: 10.4172/2161-069X-C8-086