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Articles by J. W Park
Total Records ( 4 ) for J. W Park
  S. H Lee , K. H Koo , J. W Park , H. J Kim , S. K Ye , J. B Park , B. K Park and Y. N. Kim

The plasma membrane microdomains, lipid rafts, are involved in regulation of cellular functions such as cell survival and adhesion. Cholesterol is a critical component of lipid rafts in terms of their integrity and functions and rafts disruption by cholesterol depletion can induce detachment-induced cell death. Hypoxia inducible factor-1 (HIF-1) is stabilized in hypoxia and transactivates numerous genes required for cellular adaptation to hypoxia. It is also induced by non-hypoxic stimuli and contributes to cell survival. Because hypoxia inhibits cholesterol synthesis and HIF-1 plays a role in this process, we here explored a possible connection between lipid rafts and HIF-1. We investigated whether HIF-1 is regulated during cholesterol depletion/rafts disruption in A431 cells in normoxic conditions. Methyl-beta cyclodextrin (MβCD), which induces cholesterol depletion, upregulated HIF-1 even under normoxic conditions and this upregulation required epidermal growth factor receptor (EGFR) and extracellular signal-regulated kinase 1 and 2 activation, but not Akt activation. MβCD treatment induced HIF-1 upregulation at both the transcriptional and translational levels but not at the posttranslational levels. In addition, MβCD robustly induced vascular endothelial growth factor production and stimulated an hypoxia response element-driven luciferase reporter activity under normoxic conditions, indicating that MβCD-induced HIF-1 is functionally activated. Both EGFR activity and HIF-1 expression were higher in the attached cells than in the detached cells after MβCD treatment. Furthermore, inhibition of HIF-1 by RNA interference accelerated cell detachment, thus increasing cell death, indicating that HIF-1 expression attenuates MβCD-induced anoikis-like cell death. These data suggest that, depending on cholesterol levels, lipid rafts or membrane fluidity are probably to regulate HIF-1 expression in normoxia by modulating rafts protein activities such as EGFR, and this connection between lipid rafts and HIF-1 regulation may provide cell survival under membrane-disturbing stress.

  S. G Yeo , D. Y Kim , T. H Kim , S. Y Kim , H. J Chang , J. W Park , H. S Choi and J. H. Oh

To investigate the long-term outcomes of selected patients with cT3 distal rectal cancer treated with local excision following pre-operative chemoradiotherapy.


Between January 2003 and February 2008, 11 patients with cT3 distal rectal cancer received a local excision following pre-operative chemoradiotherapy. The median age of the patients was 61 years (range, 42–71). The median tumor size was 3 cm (range, 2–5), and the median distance of the caudal tumor edge from the anal verge was 3 cm (range, 1–4). Clinical lymph node status was positive in five patients. Pre-operative chemoradiotherapy consisted of a 50.4 Gy in 28 fractions with concurrent chemotherapy. A transanal full-thickness local excision was performed after a median of 54 days (range, 31–90) from chemoradiotherapy completion. Ten patients received post-operative chemotherapy.


Pathologically complete responses occurred in eight patients, ypT1 in two and ypT2 in one. The pathologic tumor size for three ypT1–2 tumors was 0.9, 1.1 and 2.2 cm. The follow-up period was a median of 59 months (range, 24–85). One patient (ypT0) developed recurrence at the excision site 14 months after surgery, but was successfully salvaged with an abdominoperineal resection and adjuvant chemotherapy. Another patient (ypT2) developed bone metastasis after 8 months and died of the disease. The 5-year local recurrence-free, disease-free and overall survival rates were 90.9%, 81.8% and 88.9%, respectively. No Grade 3 or worse gastrointestinal toxicity was detected.


Full-thickness local excision following chemoradiotherapy may be an acceptable option for cT3 distal rectal cancer that responds well to chemoradiotherapy.

  H Zheng , J. H Nam , B Pang , D. H Shin , J. S Kim , Y. S Chun , J. W Park , H Bang , W. K Kim , Y. E Earm and S. J. Kim

Mouse B cells and their cell line (WEHI-231) express large-conductance background K+ channels (LKbg) that are activated by arachidonic acids, characteristics similar to TREK-2. However, there is no evidence to identify the molecular nature of LKbg; some properties of LKbg were partly different from the reported results of TREK type channels. In this study, we compared the properties of cloned TREK-2 and LKbg in terms of their sensitivities to ATP, phosphatidylinositol 4,5-bisphosphate (PIP2), intracellular pH (pHi), and membrane stretch. Similar to the previous findings of LKbg, TREK-2 showed spontaneous activation after membrane excision (i-o patch) and were inhibited by MgATP or by PIP2. The inhibition by MgATP was prevented by wortmannin, suggesting membrane-delimited regulation of TREKs by phosphoinositide (PI) kinase. The same was observed with the property of LKbg; the activation of TREK-2 by membrane stretch was suppressed by U73122 (PLC inhibitor). As with the known properties of TREK-2, LKbg were activated by acidic pHi and inhibited by PKC activator. Finally, we confirmed the expression of TREK-2 in WEHI-231 by using RT-PCR and immunoblot analyses. The amplitude of background K+ current and the TREK-2 expression in WEHI-231 were commonly decreased by genetic knockdown of TREK-2 using small interfering RNA. The downregulation of TREK-2 attenuated Ca2+-influx induced by arachidonic acid in WEHI-231. As a whole, these results strongly indicate that TREK-2 encodes LKbg in mouse B cells. We also newly suggest that the low activity of TREK-2 in intact cells is due to the inhibition by intrinsic PIP2.

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