• 미생물과산업
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• 제33권2호
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• pp.25-26
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• 2007

• Asian Pacific Journal of Cancer Prevention
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• 제15권11호
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• pp.4475-4482
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• 2014

Background: Cisplatin, a DNA damaging agent, induces apoptosis through increasing DNA fragmentation. However, identification of intrinsic resistance molecules against Cisplatin is vital to estimate the success of therapy. Bag-1 (Bcl-2-associated anthanogene) is one anti-apoptotic protein involved in drug resistance impacting on therapeutic efficiency. Elevated levels of this protein are related with increase cell proliferation rates, motility and also cancer development. For this reason, we aimed to understand the role of Bag-1 expression in Cisplatin-induced apoptosis in HeLa cervix cancer cells. Cisplatin decreased cell viability in time- and dose-dependent manner in wt and Bag-1L+HeLa cells. Although, $10{\mu}M$ Cisplatin treatment induced cell death within 24h by activating caspases in wt cells, Bag-1L stable transfection protected cells against Cisplatin treatment. To assess the potential protective role of Bag-1, we first checked the expression profile of interacting anti-apoptotic partners of Bag-1. We found that forced Bag-1L expression prevented Cisplatin-induced apoptosis through acting on Mcl-1 expression, which was reduced after Cisplatin treatment in wt HeLa cells. This mechanism was also supported by the regulation of heat shock protein (Hsp) family members, Hsp90 and Hsp40, which were involved in the regulation Bag-1 interactome including several anti-apoptotic Bcl-2 family members and c-Raf.

• Journal of Korean Neurosurgical Society
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• 제30권sup1호
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• pp.5-12
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• 2001

This study was designed to investigate the mechanism of cell death after cisplatin treatment in human glioblastoma A172 cells. Cis-diamminedichloroplatinum(Cisplatin) demonstrated cytostatic or cytotoxic effects on A172 cells in a dosedependent manner. Cisplatin-mediated cytotoxity in A172 cells was revealed as an apoptosis characterized by high molecular weight DNA fragmentation by agarose electrophoresis as well as nuclear fragmentation by Hoechst staining. Cisplatin also resulted in the activation of caspase 3-like protease as well as poly(ADP-ribose) polymerase(PARP) cleavage. Interestingly, the anti-apoptotic Bcl2 protein was degraded and furthermore, expression of p53 protein was increased by cisplatin in a time-dependent manner. Taken together, these results suggest that anticancer drug, cisplatin induces the apoptotic death of human glioblastoma A172 cells via the activations of caspase 3-like protease, degradation of anti-apoptotic Bcl2 protein and increase in the expression of p53.

• Journal of Microbiology and Biotechnology
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• 제12권5호
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• pp.711-715
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• 2002

Telomerase adds telomeric repeats to chromosomal ends and is known to play an important role in carcinogenesis through cellular immortalization. Since telomerase is an essential pathogenomic factor in malignant tumors, inhibiting telomerase activity is thought to be possible to make telomerase positive tumors more sensitive to cisplatin treatment, which is effective in ovarian cancers, but clinical success Is limited by chemo-resistance. In the present study, cisplatin-sensitive ovarian cancer cell line A2780 and cisplatin-resistant A2780/cp70 cell line were infected with antisense telomerase adenovirus Ad-OA. It was found that the Ad-OA suppressed ovarian cancer cell growth and this effect was mainly due to the induction of caspase-dependent apoptosis. Next, we infected the cisplatin resistant ovarian cancer cell line A2780/ cp70 with Ad-OA and cisplatin concurrently. Interestingly, cisplatin treatment with Ad-Oh was more effective to cisplatin-induced cell death in A2780/cp70 cells compared to cisplatin or the vector group only. These data suggest that cisplatin treatment with Ad-OA may be a new chemo-sensitizer for cisplatin resistant ovarian cancer.

• BMB Reports
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• 제44권3호
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• pp.211-216
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• 2011

Vitamin C (VC) is an important antioxidant and enzyme co-factor that works by stimulating the immune system and protecting against infections. It is well known that melanoma cells are more susceptible to VC than any other tumor cells. However, the role of VC in the treatment of colon cancer has not been studied. Cisplatin (CDDP) is a DNA damaging agent and is widely used for treating cancer, while the role of p53 in CDDP-induced cell death has been stressed. Using cell growth assays, morphological methods, Western blotting, flow cytometry, and DNA fragmentation analysis, we measured the expression of p53 level involved in the effect of VC on CDDP-induced apoptosis of HCT116, a human colon cancer cell line. CDDP plus VC treatment resulted in significantly increased apoptosis along with upregulation of p53 compared to untreated cells and/or CDDP-treated cells. These results suggest that VC enhanced CDDP sensitivity and apoptosis via upregulation of p53.

• 대한한의학회지
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• 제26권2호
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• pp.1-12
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• 2005

Objectives: Malignant gliomas are often treated with cisplatin (cis-diamminedichloroplatinum(II), CDDP) and radiation but results remain unsatisfactory. Since malignant glioma displays moderate resistance to conventional therapy, a new treatment modality is needed to improve the outcome of patients with these tumors. The aim of this study was to investigate the effects of the combined use of Jongjihwan(JJH) and cisplatin(CDDP) on cultured malignant glioma cells, A172. Methodss & Results: The combined use of cisplatin and Jeongjihwan had synergistic effects on Al72 cells during 24 hr-incubation, This treatment resulted in a decrease of cell viability, Which was revealed as apoptosis Characterized by activation of caspase-3 protease as well as cleavage of poly ADP-ribose polymerase (PARP) with change of mitochondria membrane potential transition. The expression of members of the Bcl-2 protein family was modulated during co-treatment with Jeongjihwan and cisplatin. Activation of caspase-3 and mitochondrial alterations were central to co-treatment with Jeongjihwan and cisplatin-induced apoptosis. Conclusions: We conclude that co-treatment with Jeongjihwan and cisplatin-induced activation of the mitochondrial pathway enables cell death. Also, we suggest the combined theory of JJH and cisplatin could be a useful method for glioblastoma.

• 대한의생명과학회지
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• 제29권3호
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• pp.178-183
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• 2023

Natural killer (NK) cells are innate cytotoxic lymphoid cells that actively prevent neoplastic development, growth, and metastatic dissemination in a process called cancer immunosurveillance. Regulation of the cytotoxic activity of NK cells relies on integrated interactions between inhibitory receptors and numerous activating receptors that act in tandem to eliminate tumor cells efficiently. Conventional chemotherapy is designed to produce an anti-proliferative or cytotoxic effect on early tumor cell division. Therapies designed to kill cancer cells and simultaneously maintain host anti-tumor immunity are attractive strategies for controlling tumor growth. Depending on the drug and dose used, several chemotherapeutic agents cause DNA damage and cancer cell death through apoptosis, immunogenic cell death, or other forms of non-killing (i.e., mitotic catastrophe, senescence, autophagy). Among stress-induced immunostimulatory proteins, changes in the expression levels of NK cell activating and inhibitory ligands and tumor cell death receptors play an important role in the detection and elimination by innate immune effectors including NK cells. Therefore, we will address how these cytotoxic lymphocytes sense and respond to high and low concentrations of drug-induced stress to the drug cisplatin, among the various types of drugs that contribute to their anticancer activity.

• 동의생리병리학회지
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• 제21권2호
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• pp.462-467
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• 2007

The radix of Pueraria thunbergiana BENTHAM (Leguminosae) is traditionally prescribed to attenuate the clinical manifestations of inner ear dysfunction and various clinical situations including fever, gastrointestinal disorders, skin problems, migraine headaches, lowering cholesterol and treating chronic alcoholism in Oriental Medicine. In the present study, we examined the effect of ethanol extract of P. thunbergiana radix (EPR) on cisplatin-mediated HEI-OC1 auditory cell death. In addition, to investingate the protection mechanism of EPR on free radicals. Treatment of EPR protected cells from cisplatin and reduced lipid peroxidation in a dose-dependent manner. Furthermore, EPR demonstrated significant scavenging activity against various free radicals, including superoxide radical, hydroxyl radical, hydrogen peroxide, and DPPH radical. These results indicate that EPR protects cisplatin-induced damages of HEI-OC1 cells through inhibition of lipid peroxidation and augmenting scavenging activities against free radials.

• 생명과학회지
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• 제24권7호
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• pp.777-783
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• 2014

항암제로 알려진 cisplatin과 t-BHP를 토끼에 투여하여 유도된 급성 신부전 시 산조인 추출액을 처리하였을 때 신장 세포의 보호에 미치는 항산화 효과를 조사하였다. 신장을 분리한 후 신피질 절편 실험에서 세포의 손상을 유발하는 지질과산화 및 LDH 실험에서 t-BHP 단독 처리 시 대조군에 비하여 각각 3배, 5배 이상 증가하였으나 산조인 추출액 0.5%를 동시 처리하였을 때는 대조군 수준으로 감소하였다. Creatinine 측정과 지질과산화 실험에서 cisplatin $5mg{\cdot}kg^{-1}$을 복강 투여한 군의 creatinine 농도가 $2.13{\pm}0.1mg{\cdot}dl^{-1}$로 나타났으나 산조인 추출액 $50mg{\cdot}kg^{-1}{\cdot}day^{-1}$을 7일간 전처리 후 cisplatin 투여 48시간 경과한 군은 $0.84{\pm}0.1mg{\cdot}dl^{-1}$로 creatinine의 농도가 약 60% 감소되는 신장보호 효과를 나타내었고, 지질과산화 검사는 cisplatin 단독 투여 시 대조군에 비하여 1.6배 높게 나타났으나 산조인 추출액 전처리 시 1.1배로 대조군과 유사하였다. 병리조직 검사는 cisplatin 단독 처리군에서 근위곱슬세관이 대조군에 대하여 더 붉게 염색되었으며 근위곱슬세관은 내강의 융모세포가 탈락하여 공포를 형성하였다. 그러나 산조인 추출액을 7일간 전처리한 군에서는 근위곱슬세관이 대조군과 유사한 염색소견을 보였고 근위곱습세관도 내강의 융모세포 탈락이 거의 나타나지 않았다. 따라서 cisplatin과 t-BHP에 의해 유발된 신장세포 손상에 대하여 산조인 추출액이 항산화 효과를 보였다.

• 생약학회지
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• 제30권3호
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• pp.255-260
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• 1999

In the previous report, E-kong-san, which is usually used for recovering health in traditional medicine, has been shown to decrease cisplatin induced nephrotoxicity in vivo and in vitro. The significant reduction of E-kong-san on the cisplatin induced nephrotoxicity led us to investigate whether the effect of this water extract was a result of triggering antioxidation. In monkey kidney Vero cells, E-kong-san at $5{\sim}10\;mg/ml$ was able to attenuate 2mM cisplatin-stimulated cell death by 46.8% and 31.8%, respectively. E-kong-san showed strong free radical scavengering activities on 1,1-diphenyl-2-picrylhydrazil (DPPH) radical and xanthine/xanthine oxidase (XOD) generated superoxide anion radical $(O_2^{-.})$. We further studied the effects of E-kong-san on lipid peroxidation in rat liver microsomes induced by enzymatic and nonenzymatic methods. Moreover, E-kong-san exhibited significant inhibition on both ascorbic $acid/Fe^{2+}$ and $ADP/NADPH/Fe^{3+}$ induced lipid peroxidation in rat liver microsomes. Based on these results, we suggest that E-kong-san protects the cisplatin induced cytotoxicity by its antioxidative mechanism.