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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.com

Priyanca Ahlawat, J Gastrointest Dig Syst 2018, Volume 8

DOI: 10.4172/2161-069X-C8-086