Effect of Pancreatic Cancer Cell-Derived Extracellular Vesicle on Normal Hepatocyte

Abstract

Abstract Effect of Pancreatic Cancer Cell-Derived Extracellular Vesicle on Normal hepatocyte

AHN JAESUNG The Graduate Schoool of Hanyang University (Directed by Professor Ju Seop Kang, M.D., PhD)

Back ground : Extracelluar vesicles(EV) are small membranous vesicles that imply exosomes, ectosomes, oncosomes and microvesicle. They have similar role in the interior of the body but different in size. EV contains a variety of proteins, nucleic acid, lipid and miRNA, and those have important role in cell to cell communication. Tumor-derived EV are main mediators of intercellular communication and are known to make microenvironment for cancer metastasis. Cancer cell invasion through blood vessels or lymph node, also known as homing, is an influential theory.

Methods: E-cadherin is a marker for epitherial cells, which means it has not yet changed into cancer. There is a theory that tumor-secreted EV can play a role in epithelial messenchymal transition (EMT). Briefly, when EMT initiates, cancer metastasis cascade also starts. That is the reason that E-cadherin, epithelial marker, level has been checked in the experiment. The study was performed in 3 phases. First of all, normal hepatocyte and pancreatic cancer cell was co-cultured in order to see if metastasis occurs. And then E-cadherin level was detected by ELISA. Lastly, tumor suppressor gene p53 on co-cultured normal hepatocyte was verified through reverse transcription PCR.

Result : The E-cadherin level of co-cultured group became lower compared of normal group. Compared to 3 day treated group, 6 day treated group had lower E-cadherin level. On the other hand, the p53 level of both co-cultured group and cancer group shown increase compared to normal group.

Conclusion: There is a pancreatic cancer metastasis pathway other than homing theory, which is known to be a common pathway, and is a theory that cancer cell moves. However, in my theory, EV alone has effect on metastasis. In my experiment condition, there was no microenvironment which helped cancer cell to migrate. Instead, there was only exchange of EV between pancreatic cancer cells and hepatocytes.

Keywords: Extracellular vesicles, Metastasis, Pancreatic cancer cell, Hepatocyte