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Epigenetic Activation of Tensin 4 Promotes Gastric Cancer Progression
Mirang Kim,Haejeong Heo,Hee-Jin Kim,Keeok Haam,Hyun Ahm Sohn,Yang-Ji Shin,Hanyong Go,Hyo-Jung Jung,Jong-Hwan Kim,Sang-Il Lee,Kyu-Sang Song,Min-Ju Kim,Haeseung Lee,Eun-Soo Kwon,Seon-Young Kim,Yong Sung 한국분자세포생물학회 2023 Molecules and cells Vol.46 No.5
Gastric cancer (GC) is a complex disease influenced by multiple genetic and epigenetic factors. Chronic inflammation caused by Helicobacter pylori infection and dietary risk factors can result in the accumulation of aberrant DNA methylation in gastric mucosa, which promotes GC development. Tensin 4 (TNS4), a member of the Tensin family of proteins, is localized to focal adhesion sites, which connect the extracellular matrix and cytoskeletal network. We identified upregulation of TNS4 in GC using quantitative reverse transcription PCR with 174 paired samples of GC tumors and adjacent normal tissues. Transcriptional activation of TNS4 occurred even during the early stage of tumor development. TNS4 depletion in GC cell lines that expressed high to moderate levels of TNS4, i.e., SNU-601, KATO III, and MKN74, reduced cell proliferation and migration, whereas ectopic expression of TNS4 in those lines that expressed lower levels of TNS4, i.e., SNU-638, MKN1, and MKN45 increased colony formation and cell migration. The promoter region of TNS4 was hypomethylated in GC cell lines that showed upregulation of TNS4. We also found a significant negative correlation between TNS4 expression and CpG methylation in 250 GC tumors based on The Cancer Genome Atlas (TCGA) data. This study elucidates the epigenetic mechanism of TNS4 activation and functional roles of TNS4 in GC development and progression and suggests a possible approach for future GC treatments.
Mirang Lee,Youngmin Han,Jae Seung Kang,Yoo Jin Choi,Hee Ju Sohn,Wooil Kwon,Jin-Young Jang 대한외과학회 2024 Annals of Surgical Treatment and Research(ASRT) Vol.106 No.1
Purpose: In the era of minimally invasive surgery (MIS), robotic pancreatoduodenectomy (PD) is actively performed, and clinical fellows need to thoroughly prepare for MIS-PD during the training process. Although pancreaticojejunostomy (PJ) is a difficult anastomosis that requires repeated practice, there are obstacles preventing its practice that concerns patient safety and limited time in the actual operating room. This study evaluated the efficacy of simulation-based training of robotic duct-to-mucosa PJ using pancreatic and intestinal silicone models using a scoring system. Methods: Three pancreatobiliary clinical fellows who had never performed a real robotic PJ participated in this study. Each trainee, who was well acquainted with master’s video created by a senor surgeon, performed the robotic PJ procedures 9 times, and 3 independent pancreatobiliary surgeons assessed the videos and analyzed the scores using a blind method. Results: The mean robotic PJ times for the 3 trainees were 42.8 and 29.1 minutes for the first and 9th videos, respectively. The mean score was 13.8 (range, 6–17) for the first video and 17.7 (range, 15–19) for the 9th video. When comparing earlier and later attempts, the PJ time decreased significantly (2,201.67 seconds vs. 2,045.50 seconds, P = 0.007), whereas test scores increased significantly (total score 14.22 vs. 16.89, P = 0.011). Conclusion: This robotic education system will help pancreatobiliary trainees overcome the learning curves efficiently and quickly without raising ethical concerns associated with animal models or direct practice with human subjects. This will be of practical assistance to trainees preparing for MIS-PD.
Kim, Mirang,Park, Young-Kyu,Kang, Tae-Wook,Lee, Sang-Hun,Rhee, Yong-Hee,Park, Jong-Lyul,Kim, Hee-Jin,Lee, Daeyoup,Lee, Doheon,Kim, Seon-Young,Kim, Yong Sung Oxford University Press 2014 Human Molecular Genetics Vol.23 No.3
<P>DNA methylation and hydroxymethylation have been implicated in normal development and differentiation, but our knowledge is limited about the genome-wide distribution of 5-methylcytosine (5 mC) and 5-hydroxymethylcytosine (5 hmC) during cellular differentiation. Using an <I>in vitro</I> model system of gradual differentiation of human embryonic stem (hES) cells into ventral midbrain-type neural precursor cells and terminally into dopamine neurons, we observed dramatic genome-wide changes in 5 mC and 5 hmC patterns during lineage commitment. The 5 hmC pattern was dynamic in promoters, exons and enhancers. DNA hydroxymethylation within the gene body was associated with gene activation. The neurogenesis-related genes <I>NOTCH1</I>, <I>RGMA</I> and <I>AKT1</I> acquired 5 hmC in the gene body and were up-regulated during differentiation. DNA methylation in the promoter was associated with gene repression. The pluripotency-related genes <I>POU5F1</I>, <I>ZFP42</I> and <I>HMGA1</I> acquired 5 mC in their promoters and were down-regulated during differentiation. Promoter methylation also acted as a locking mechanism to maintain gene silencing. The mesoderm development-related genes <I>NKX2-8</I>, <I>TNFSF11</I> and <I>NFATC1</I> acquired promoter methylation during neural differentiation even though they were already silenced in hES cells. Our findings will help elucidate the molecular mechanisms underlying lineage-specific differentiation of pluripotent stem cells during human embryonic development.</P>