z-logo
Premium
Differential bacterial invasion in normal and cancer hepatocytes
Author(s) -
Hong Jung Woo,
Kim Mina,
Song Sukhyun,
Shin Jennifer Hyunjong
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1217.9
Subject(s) - myosin , actin , cancer cell , cytoskeleton , microbiology and biotechnology , biology , western blot , gentamicin protection assay , cancer , cell , biochemistry , gene , genetics
Despite numerous demonstrations of bacteria targeting and reducing tumor by inducing necrosis in several animal studies, the actual mechanisms of bacteria targeting and invading into cancer remain unclear. In this study, the differential bacterial invasion and necrosis in cancer and normal hepatocytes were analyzed using Salmonella typhimurium . Observations of bacteria exhibiting selective targeting for cancer hepatocytes (HepG2) over normal hepatocytes (THLE‐2) were made initially with a novel microfluidic platform. When cells were infected directly, cancer cells were more vulnerable to infection than normal cells, resulting in much lower survival after 90 minutes. Cancer cells featured more prominent alterations in cytoskeletal actin, indicating the importance of actin related proteins in invasion. Since myosin II plays critical roles in regulating actin filaments, we treated cells with blebbistatin and calyculin A to inhibit and enhance the activity of myosin II, respectively. Blebbistatin treatment greatly enhanced cell survival while calyculin A lowered the survival of cells against infection, signifying myosin II activity in bacterial invasion. Western blot analysis confirmed higher intrinsic level and activity of myosin II in HepG2 than THLE‐2 suggesting that the vulnerability of HepG2 against bacterial infection depends on the inherently high level of myosin II and its activity.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here