Sun-Mi Lee

Adiponectin and adiponectin receptor in relation to colorectal cancer progression

Although obesity is a risk factor for colorectal cancer, the underlying mechanism is not clear. Adiponectin is an adipokine that binds to 2 types of receptors, AdipoR1 and AdipoR2. The plasma concentrations of adiponectin are reduced in obese individuals and adiponectin has been reported to have anticarcinogenic properties. Furthermore, AdipoR1 and AdipoR2 have been reported to be expressed in several malignancies. However, little is known about the expression of AdipoR1 and AdipoR2 in colorectal cancer and its clinicopathological implications. In addition, the relationship between adiponectin and colorectal cancer has not yet been determined. Here, we sought to investigate adiponectin and adiponectin receptors in relation to colorectal cancer. AdipoR1 and AdipoR2 immunostaining was detected in 72 and 68% of human colorectal cancer tissue, respectively. AdipoR1 and AdipoR2 expression levels were inversely related to T stage. The lowest AdipoR1 and AdipoR2 expression were detected in poorly differentiated adenocarcinoma. RT‐PCR also showed the expression of AdipoR1 and AdipoR2 in HCT116 and SW620. MTT assay and TUNEL assay demonstrated the tendency of growth inhibition and apoptosis induction in both cell lines after full‐length adiponectin treatment although statistically insignificant. Microarray analysis revealed several gene responses to full‐length adiponectin, including upregulation of ENDOGL1 and MT1G. In conclusion, AdipoR1 and AdipoR2 may be intimately related to the progression of colorectal cancer. Further studies may be warranted to assess adiponectin and its receptors as a novel target for inhibition of colorectal cancer growth.

Pre-operative transarterial chemoembolization for resectable hepatocellular carcinoma adversely affects post-operative patient outcome.

Background Long‐term outcomes after hepatic resection for hepatocellular carcinoma are not satisfactory because of high recurrence rates.

Clinical usefulness of telomerase for the detection of colon cancer in ulcerative colitis patients

Background and Aim: Colorectal carcinoma (CRC) is a complication of ulcerative colitis (UC). Although stool occult blood and colonoscopy are used to detect CRC in UC, these methods have drawbacks, in that bleeding is associated with UC and the underlying mucosa is irregular, making it difficult to detect dysplasia. Telomerase and its catalytic subunit, telomerase reverse transcriptase (hTERT), are specifically expressed in cancers, making them candidate markers for the early detection of cancer. We previously reported that assays of telomerase in pancreatic juice may be useful for the early detection of pancreatic cancer. The aims of our study were to determine whether assays for telomerase and TERT may be useful in the diagnosis of CRC developed in UC patients.

The Helicobacter pylori Mfd protein is important for antibiotic resistance and DNA repair

A Helicobacter pylori mutant defective in a putative mfd gene was constructed and characterized. The mfd gene is required for DNA repair and is involved in DNA recombination processes. The mfd mutant strain displayed a greatly increased susceptibility to antibiotics, indicating that this gene plays a significant role in the antibiotic resistance of H. pylori strain J99.

Mechanism of Metronidazole Resistance Regulated by the fdxA Gene in Helicobacter pylori.

Resistance to metronidazole in Helicobacter pylori results from inactivation of rdxA and frxA, the chromosomal genes for a nitroreductase that normally converts metronidazole from prodrug to bactericidal agent. Two types of metronidazole susceptible strains had been found distinguishable by their apparent levels of frxA expression. Most common in the populations we had studied were strains that required only rdxA inactivation to become resistant to moderate levels of metronidazole(type I strains). The second strain type required inactivation of both frxA and rdxA to become resistance to metronidazole(type II strains): this was linked to a relatively high level of frxA gene transcription in the type II strains. The fdxA gene regulated fdxA as well as rdxA gene. Thus, to study the function of fdxA as a regulatory gene we constructed a null mutant of fdxA in H. pylori genome and identified over-and under-expressed proteins by fdxA using two-dimensional(2-D) electrophoresis and MALDI-TOP-MS. There were four over-expressed proteins in fdxA mutant; nifU-like protein(HP0221), frxA(HP0642), nonheme ferritin(HP0653), and hypothetical protein(HP0902). Three under-expressed proteins were also identified in fdxA mutant, including 5`-methylthioadenosine/S-adenosylhomocysteine nucleosidase (HP0089), (3R)-hydroxymyristoyl ACP dehydratase(HP1376), and thioredoxin(HP1458).

15-Hydroxyprostaglandin dehydrogenase as a marker in colon carcinogenesis: analysis of the prostaglandin pathway in human colonic tissue

Background/Aims Cyclooxygenase-2 (COX-2), 15-hydroxyprostaglandin dehydrogenase (15-PGDH), and microsomal prostaglandin E synthase-1 (mPGEs-1) regulate prostaglandin E2 (PGE2) expression and are involved in colon carcinogenesis. We investigated the expression of PGE2 and its regulating genes in sporadic human colon tumors and matched normal tissues. Methods Twenty colonic adenomas and 27 colonic adenocarcinomas were evaluated. COX-2 and 15-PGDH expression was quantified by real-time polymerase chain reaction. The expression of PGE2 and mPGEs-1 was measured using enzyme-linked immunosorbent assay and Western blotting, respectively. Results The expression of COX-2, mPGEs-1, and PGE2 did not differ between the adenomas and matched distant normal tissues. 15-PGDH expression was lower in adenomas than in the matched normal colonic tissues (P<0.001). In adenocarcinomas, mPGEs-1 and PGE2 expression was significantly higher (P<0.001 and P=0.020, respectively), and COX-2 expression did not differ from that in normal tissues (P=0.207). 15-PGDH expression was significantly lower in the normal colonic mucosa from adenocarcinoma patients than in the normal mucosa from adenoma patients (P=0.018). Conclusions Early inactivation of 15-PGDH, followed by activation of COX-2 and mPGEs-1, contributes to PGE2 production, leading to colon carcinogenesis. 15-PGDH might be a novel candidate marker for early detection of field defects in colon carcinogenesis.