Seoul National UniversitySeoul Republic of Korea

Seoul National UniversitySeoul Republic of Korea

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Bach D.-H.,Seoul National UniversitySeoul Republic of Korea | Hong J.-Y.,Seoul National UniversitySeoul Republic of Korea | Park H.J.,Seoul National UniversitySeoul Republic of Korea | Lee S.K.,Seoul National UniversitySeoul Republic of Korea
International Journal of Cancer | Year: 2017

Chemotherapy, one of the principal approaches for cancer patients, plays a crucial role in controlling tumor progression. Clinically, tumors reveal a satisfactory response following the first exposure to the chemotherapeutic drugs in treatment. However, most tumors sooner or later become resistant to even chemically unrelated anticancer agents after repeated treatment. The reduced drug accumulation in tumor cells is considered one of the significant mechanisms by decreasing drug permeability and/or increasing active efflux (pumping out) of the drugs across the cell membrane. The mechanisms of treatment failure of chemotherapeutic drugs have been investigated, including drug efflux, which is mediated by extracellular vesicles (EVs). Exosomes, a subset of EVs with a size range of 40-150 nm and a lipid bilayer membrane, can be released by all cell types. They mediate specific cell-to-cell interactions and activate signaling pathways in cells they either fuse with or interact with, including cancer cells. Exosomal RNAs are heterogeneous in size but enriched in small RNAs, such as miRNAs. In the primary tumor microenvironment, cancer-secreted exosomes and miRNAs can be internalized by other cell types. MiRNAs loaded in these exosomes might be transferred to recipient niche cells to exert genome-wide regulation of gene expression. How exosomal miRNAs contribute to the development of drug resistance in the context of the tumor microenvironment has not been fully described. In this review, we will highlight recent studies regarding EV-mediated microRNA delivery in formatting drug resistance. We also suggest the use of EVs as an advancing method in antiresistance treatment. © 2017 UICC.

Jang Y.-S.,Gachon UniversityIncheon Republic of Korea | Kang J.-H.,Gachon UniversityIncheon Republic of Korea | Woo J.K.,Gachon UniversityIncheon Republic of Korea | Kim H.M.,Gachon UniversityIncheon Republic of Korea | And 4 more authors.
International Journal of Cancer | Year: 2016

Nerve injury-induced protein 1 (Ninjurin1, Ninj1) is a cell surface molecule that can mediate homophilic adhesion and promote neurite outgrowth from cultured dorsal root ganglion (DRG) neurons. Interestingly, Ninj1 overexpressed in human cancer; however, its role in metastasis is not clear. This study showed that inhibition of Ninj1 promotes lung cancer metastasis through interleukin 6 (IL-6)/STAT3 signaling. Ninj1 levels were relatively low in highly motile lung cancer cells. While inhibition of Ninj1 enhanced cell migration in lung cancer cells, overexpression of Ninj1 significantly suppressed it. We found that inhibition of Ninj1 significantly increased expression and secretion of IL-6 in A549 cells. We also found that inhibition of IL-6 decreased intercellular adhesion molecule 1 (ICAM-1) expression. In addition, inhibition of Ninj1 significantly increased cell motility and invasiveness of lung cancer cells. In an in vivo model, we found that Ninj1 suppression did not affect tumor growth but induced significant increase in incidence of lung metastasis, and sizes and number of tumor nodules. Taken together, our data clearly demonstrate that Ninj1 suppresses migration, invasion and metastasis of lung cancer via inhibition of the IL-6 signaling pathway in vitro and in vivo. © 2016 UICC.

Richards K.J.,Pacific University in Oregon | Natarov A.,Hawaii Pacific University | Firing E.,University of Hawaii at Manoa | Kashino Y.,Research Institute for Global Change | And 5 more authors.
Journal of Geophysical Research C: Oceans | Year: 2015

We investigate the characteristics of shear-generated turbulence in the natural environment by considering data from a number of cruises in the western equatorial Pacific. In this region, the vertical shear of the flow is dominated by flow structures that have a relatively small vertical scale of O(10 m). Combining data from all cruises, we find a strong relationship between the turbulent dissipation rate, ε{lunate}, vertical shear, S, and buoyancy frequency, N. Examination of ε{lunate} at a fixed value of Richardson number, Ri=N2/S2, shows that ε{lunate}∝ut2N for a wide range of values of N, where ut is an appropriate velocity scale which we assume to be the horizontal velocity scale of the turbulence. The implied vertical length scale, ℓv=ut/N, is consistent with theoretical and numerical studies of stratified turbulence. Such behavior is found for Ri<0.4. The vertical diffusion coefficient then scales as κv∝ut2/N at a fixed value of Richardson number. The amplitude of ε{lunate} is found to increase with decreasing Ri, but only modestly, and certainly less dramatically than suggested by some parameterization schemes. Provided the shear generating the turbulence is resolved, our results point to a way to parameterize the unresolved turbulence. © 2015. American Geophysical Union. All Rights Reserved.

Yeo J.-H.,Kyung Hee UniversitySeoul Republic of Korea | Yoon S.-Y.,Seoul National UniversitySeoul Republic of Korea | Kim S.-J.,Kyung Hee UniversitySeoul Republic of Korea | Oh S.-B.,Seoul National UniversitySeoul Republic of Korea | And 3 more authors.
International Journal of Cancer | Year: 2016

Cancer chemotherapy with platinum-based antineoplastic agents including oxaliplatin frequently results in a debilitating and painful peripheral neuropathy. We evaluated the antinociceptive effects of the alpha-2 adrenoceptor agonist, clonidine on oxaliplatin-induced neuropathic pain. Specifically, we determined if (i) the intraperitoneal (i.p.) injection of clonidine reduces mechanical allodynia in mice with an oxaliplatin-induced neuropathy and (ii) concurrent inhibition of p38 mitogen-activated protein kinase (MAPK) activity by the p38 MAPK inhibitor SB203580 enhances clonidine's antiallodynic effect. Clonidine (0.01-0.1 mg kg-1, i.p.), with or without SB203580(1-10 nmol, intrathecal) was administered two weeks after oxaliplatin injection(10 mg kg-1, i.p.) to mice. Mechanical withdrawal threshold, motor coordination and blood pressure were measured. Postmortem expression of p38 MAPK and ERK as well as their phosphorylated forms(p-p38 and p-ERK) were quantified 30 min or 4 hr after drug injection in the spinal cord dorsal horn of treated and control mice. Clonidine dose-dependently reduced oxaliplatin-induced mechanical allodynia and spinal p-p38 MAPK expression, but not p-ERK. At 0.1 mg kg-1, clonidine also impaired motor coordination and decreased blood pressure. A 10 nmol dose of SB203580 alone significantly reduced mechanical allodynia and p-p38 MAPK expression, while a subeffective dose(3 nmol) potentiated the antiallodynic effect of 0.03 mg kg-1 clonidine and reduced the increased p-p38 MAPK. Coadministration of SB203580 and 0.03 mg kg-1 clonidine decreased allodynia similar to that of 0.10 mg kg-1 clonidine, but without significant motor or vascular effects. These findings demonstrate that clonidine treatment reduces oxaliplatin-induced mechanical allodynia. The concurrent administration of SB203580 reduces the dosage requirements for clonidine, thereby alleviating allodynia without producing undesirable motor or cardiovascular effects. © 2015 UICC.

Oh K.-Y.,Seoul National UniversitySeoul Republic of Korea | Kang K.-R.,Seoul National UniversitySeoul Republic of Korea | Yoon H.-J.,Seoul National UniversitySeoul Republic of Korea | Lee J.-I.,Seoul National UniversitySeoul Republic of Korea | And 2 more authors.
Head and Neck | Year: 2016

Background: Granular cell tumor (GCT) is a benign soft tissue tumor of neural origin and is characterized by eosinophilic granular cells showing positivity for neuronal markers. Herein, we report the first case of primary intraosseous GCT arising in the maxilla of an adolescent girl. Methods and Results: A 16-year-old female patient presented with palatal swelling. Radiographic findings revealed a well-defined radiolucent lesion centrally located in the right maxilla. Mass excision was performed, and histopathologic examination showed sheets and cords of eosinophilic granular cells with cellular pleomorphism. Tumor cells were strongly positive for vimentin, S-100 protein, and CD56, and negative for cytokeratin, desmin, smooth muscle actin, and c-kit. High expression of p53 and Ki-67 was found. The final diagnosis was atypical GCT. Conclusion: When evaluating an intraosseous radiolucent lesion with histopathologic features of granular cells, clinicians and pathologists should include GCT in the differential diagnosis. © 2016 Wiley Periodicals, Inc.

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