Journal of Microbiology

Research Support, Non-U.S. Gov't

Effect of Salmonella Treatment on an Implanted Tumor (CT26) in a Mouse Model: Misun Yun , SangO Pan , Sheng- Nan Jiang , Vu Hong Nguyen , Seung-Hwan Park , Che-Hun Jung , Hyung-Seok Kim , Jung-Joon Min , Hyon E. Choy , Yeongjin Hong; J. Microbiol. 2012;50(3):502-510. Published online June 30, 2012; DOI: https://doi.org/10.1007/s12275-012-2090-9

Abstract: The use of bacteria has contributed to recent advances in targeted cancer therapy especially for its tumor-specific accumulation and proliferation. In this study, we investigated the molecular events following bacterial therapy using an attenuated Salmonella Typhimurium defective in ppGpp synthesis (ΔppGpp), by analyzing those proteins differentially expressed in tumor tissues from treated and untreated mice. CT26 murine colon cancer cells were implanted in BALB/c mice and allowed to form tumors. The tumor-bearing mice were treated with the attenuated Salmonella Typhimurium. Tumor tissues were analyzed by 2D-PAGE. Fourteen differentially expressed proteins were identified by mass spectrometry. The analysis revealed that cytoskeletal components, including vimentin, drebrin-like protein, and tropomyosinalpha 3, were decreased while serum proteins related to heme or iron metabolism, including transferrin, hemopexin, and haptoglobin were increased. Subsequent studies revealed that the decrease in cytoskeletal components occurred at the transcriptional level and that the increase in heme and iron metabolism proteins occurred in liver. Most interestingly, the same pattern of increased expression of transferrin, hemopexin, and haptoglobin was observed following radiotherapy at the dosage of 14 Gy.

Journal Article

Hepatitis C Virus Non-structural Protein NS4B Can Modulate an Unfolded Protein Response: Yi Zheng , Bo Gao , Li Ye , Lingbao Kong , Wei Jing , Xiaojun Yang , Zhenghui Wu , Linbai Ye; J. Microbiol. 2005;43(6):529-536.; DOI: https://doi.org/2294 [pii]

Abstract: Viral infection causes stress to the endoplasmic reticulum (ER). The response to endoplasmic reticulum stress, known as the unfolded protein response (UPR), is designed to eliminate misfolded proteins and allow the cell to recover. The role of hepatitis C virus (HCV) non-structural protein NS4B, a component of the HCV replicons that induce UPR, is incompletely understood. We demonstrate that HCV NS4B could induce activating transcription factor (ATF6) and inositol-requiring enzyme 1 (IRE1), to favor the HCV subreplicon and HCV viral replication. HCV NS4B activated the IRE1 pathway, as indicated by splicing of X box-binding protein (Xbp-1) mRNA. However, transcriptional activation of the XBP-1 target gene, EDEM (ER degradation-enhancing a-mannosidase-like protein, a protein degradation factor), was inhibited. These results imply that NS4B might induce UPR through ATF6 and IRE1-XBP1 pathways, but might also modify the outcome to benefit HCV or HCV subreplicon replication.

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