Publications by authors named "Ju-Hwa Kim"

The prognostic and therapeutic relevance of molecular subtypes for the most aggressive isocitrate dehydrogenase 1/2 (IDH) wild-type glioblastoma (GBM) is currently limited due to high molecular heterogeneity of the tumors that impedes patient stratification. Here, we describe a distinct binary classification of IDH wild-type GBM tumors derived from a quantitative proteomic analysis of 39 IDH wild-type GBMs as well as IDH mutant and low-grade glioma controls. Specifically, GBM proteomic cluster 1 (GPC1) tumors exhibit Warburg-like features, neural stem-cell markers, immune checkpoint ligands, and a poor prognostic biomarker, FKBP prolyl isomerase 9 (FKBP9).

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Objective: To propose a new anthropometric index that can be employed to better predict percent body fat (PBF) among young adults and to compare with current anthropometric indices.

Design: Cross-sectional.

Setting: All measurements were taken in a controlled laboratory setting in Seoul (South Korea), between 1 December 2015 and 30 June 2016.

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Diversity in the genetic lesions that cause cancer is extreme. In consequence, a pressing challenge is the development of drugs that target patient-specific disease mechanisms. To address this challenge, we employed a chemistry-first discovery paradigm for de novo identification of druggable targets linked to robust patient selection hypotheses.

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Background/aim: Colchicine (COL) is a well-known and potent microtubule targeting anticancer agent. The purpose of our study was to identify conditions that increase sensitization of COL-resistant cancer cells that overexpress P-glycoprotein (P-gp).

Materials And Methods: The anti-malarial drugs chloroquine (CHL), mefloquine (MEF) and primaquine (PRI) have been shown to increase sensitization in drug-resistant KBV20C cells via P-gp inhibition.

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Article Synopsis
  • - Clinical trials are evaluating AZD5363, an AKT inhibitor, for its impact on the PI3K/AKT/mTOR pathway, noting that cancer cells may activate alternative growth pathways when inhibited.
  • - In experiments with Hs578T breast cancer cells, AZD5363 treatment led to a decrease in pGSK3β but an increase in activated pAKT, which is linked to cancer growth; researchers aimed to find ways to reduce this pAKT increase.
  • - Co-treating with PI3K/AKT/mTOR inhibitors like LY294002 or MK-2206 alongside AZD5363 effectively reduced pAKT levels, suggesting that combining MK-2206 with AZD
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The purpose of this study was to identify conditions that would increase the sensitivity of drug-resistant cancer cells. Previously, two anti-malarial drugs, chloroquine (CHL) and primaquine (PRI), showed different sensitization effects for vinblastine (VIB)-resistant cancer cells. Herein, we tested co-treatment of cells with CHL or PRI and other microtubule-targeting cancer drugs, namely, vinorelbine (VIO), paclitaxel (PAC), docetaxel (DOC), vincristine (VIC), or halaven (HAL).

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Undesirable toxicity is one of the main reasons for withdrawing drugs from the market or eliminating them as candidates in clinical trials. Although numerous studies have attempted to identify biomarkers capable of predicting pharmacotoxicity, few have attempted to discover robust biomarkers that are coherent across various species and experimental settings. To identify such biomarkers, we conducted meta-analyses of massive gene expression profiles for 6,567 in vivo rat samples and 453 compounds.

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Article Synopsis
  • * The study found that combining AZD5363 with low levels of salinomycin effectively reduces the growth of breast cancer cells by promoting apoptosis and S-phase arrest.
  • * These findings suggest that salinomycin could enhance the effectiveness of AZD5363, potentially leading to better cancer treatment options in the future.
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MK-2206 is an inhibitor of Akt activation. It has been investigated as an anticancer drug in clinical trials assessing the potential of pAkt targeting therapy. The purpose of this study was to identify conditions that increase the sensitivity of cancer cells to MK-2206.

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This study was designed to identify conditions that induce an increase in the sensitivity of drug-resistant cancer cells compared to sensitive cells. Using cell proliferation assays and microscopic observation, thioridazine (THIO) was found to induce higher sensitization in drug-resistant KBV20C cancer cells compared to sensitive KB parent cells. By studying cleaved PARP, annexin V staining, and Hoechst staining, we found that THIO largely increased apoptosis specifically in KBV20C cells, suggesting that the difference in sensitization between the resistant and sensitive cells can be attributed to the ability of THIO to induce apoptosis.

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The purpose of this study was to identify conditions that increase the sensitivity of resistant cancer cells to antimitotic drugs. Using MTS assays, microscopic observation, assessment of cleaved PARP, FACS analysis, and Hoechst staining, we found that the c-Jun N-terminal kinase (Jnk) inhibitor SP600125 (SP) sensitized the antimitotic drug-resistant KBV20C cancer cell line. The sensitization mechanism was independent of p-glycoprotein (P-gp) inhibition.

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The purpose of this study was to identify conditions that will increase the sensitivity of resistant cancer cells to anti-mitotic drugs. Currently, atovaquine (ATO), chloroquine (CHL), primaquine (PRI), mefloquine (MEF), artesunate (ART), and doxycycline (DOY) are the most commonly used anti-malarial drugs. Herein, we tested whether anti-malarial drugs can sensitize drug-resistant KBV20C cancer cells.

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The present study identified a novel salinomycin (Sal)-sensitization mechanism in cancer cells. We analyzed the signal proteins Akt, Jnk, p38, Jak, and Erk1/2 in cancer cell lines that had arrested growth following low amounts of Sal treatment. We also tested the signal molecules PI3K, PDK1, GSK3β, p70S6K, mTOR, and PTEN to analyze the PI3K/Akt/mTOR pathway.

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The present study identified a novel salinomycin (Sal) sensitization mechanism in cancer. We tested whether Sal reduced proliferation in a high-density population by counting attached cell numbers after Sal treatment. Sal reduced proliferation in high-density cell populations.

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In this study, we synthesized a novel carbazole derivative, MHY407, as a sensitizer of cancer cells to increase DNA damage. We then evaluated the anticancer effects of MHY407 and identified the molecular mechanism for the sensitization of breast cancer cell lines. MHY407 significantly increased DNA damage as determined by DNA breakage, levels of damage-responsive proteins, and DNA foci.

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Here, we investigated whether Sal could sensitize cancer cells to antimitotic drugs. We demonstrated that Sal sensitized paclitaxcel (PAC)-, docetaxcel (DOC)-, vinblastin (VIN)-, or colchicine (COL)-treated cancer cell lines, suggesting that Sal has the ability to sensitize the cells to any form of microtubule-targeting drugs. Sensitization to the antimitotic drugs could be achieved with very low concentrations of Sal, suggesting that there is a possibility to minimize Sal toxicity associated with human cancer patient treatments.

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In the present study, we investigated mRNA expression patterns of both SOCS5 and SOCS6 in various normal and cancer tissues using a commercially available Cancer Profiling Array. We found that SOCS5 and SOCS6 had similar expression patterns in most cancer and healthy individuals, suggesting that these two genes are transcriptionally co-regulated. Tissue-specific up- or down-regulation of SOCS5 and SOCS6 was observed in several cancer tissues.

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Salinomycin (Sal) is potentially useful for the treatment of cancer. The present study examined a novel mechanism of Sal sensitization in cancer cells. Sal sensitized radiation-treated cancer cells by inducing G2 arrest and causing DNA damage.

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Background And Purpose: Salinomycin (Sal) has recently been shown to inhibit various cancer stem cells. Here, we investigated whether Sal could sensitize cancer cells to the effects of doxorubicin (DOX) or etoposide (ETO).

Experimental Approach: Using the Comet assay, immunocytochemistry and Western blot analysis, we assessed the ability of Sal to increase DNA breakage.

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We sought to identify altered transcription factors (Stat, AP1, and NF-kB) or signal proteins (Erk1/2, p38, Akt, Jnk, Jak, and c-Src) in cancer cell lines whose growth was arrested by doxorubicin (DOX) treatment. Jnk1 was the only signal protein to be activated. DOX increased Stat3 phosphorylation, nuclear localization, and transcriptional activity.

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We identified four breast cancer cell lines and one stomach cancer cell line resistant to the cytotoxic effects of doxorubicin (DOX) and examined their sensitivity to other chemotherapeutic agents. SP600125, an inhibitor of the Jnk pathway, reduced the cellular viability of all five DOX-resistant cancer cell lines. Jnk1 siRNA also reduced the viability of the one DOX-resistant cell line in which it was tested.

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