• Journal of Korean Neurosurgical Society
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• 제53권4호
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• pp.228-234
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• 2013

Objective : We have limited understanding on the presentation and survival of primary spinal sarcomas. The survival, recurrence rate, and related prognostic factors were investigated after treatment for primary sarcomas of the spine. Methods : Retrospective analysis of medical records and radiological data was done for 29 patients in whom treatment was performed due to primary sarcoma of the spine from 2000 to 2010. As for treatment method, non-radical operation, radiation therapy, and chemotherapy were simultaneously or sequentially combined. Overall survival (OS), progression free survival (PFS), ambulatory function, and pain status were analyzed. In addition, factors affecting survival and recurrence were analyzed : age (${\leq}42$ or ${\geq}43$), gender, tumor histologic type, lesion location (mobile spine or rigid spine), weakness at diagnosis, pain at diagnosis, ambulation at diagnosis, initial treatment, radiation therapy, kind of irradiation, surgery, chemotherapy and distant metastasis. Results : Median OS was 60 months, the recurrence rate was 79.3% and median PFS was 26 months. Patients with distant metastasis showed significantly shorter survival than those without metastasis. No factors were found to be significant relating to recurrence. Prognostic factor associated with walking ability was the presence of weakness at diagnosis. Conclusion : Primary spinal sarcomas are difficult to cure and show high recurrence rate. However, the development of new treatment methods is improving survival.

• BMB Reports
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• 제48권2호
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• pp.109-114
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• 2015

The COX-2/$PGE_2$ pathway has been implicated in the occurrence and progression of cancer. The underlying mechanisms facilitating the production of COX-2 and its mediator, $PGE_2$, in cancer survival remain unknown. Herein, we investigated $PGE_2$-induced COX-2 expression and signaling in HL-60 cells following menadione treatment. Treatment with $PGE_2$ activated anti-apoptotic proteins such as Bcl-2 and Bcl-xL while reducing pro-apoptotic proteins, thereby enhancing cell survival. $PGE_2$ not only induced COX-2 expression, but also prevented casapse-3, PARP, and lamin B cleavage. Silencing and inhibition of COX-2 with siRNA transfection or treatment with indomethacin led to a pronounced reduction of the extracellular levels of $PGE_2$, and restored the menadione- induced cell death. In addition, pretreatment of cells with the MEK inhibitor PD98059 and the PKA inhibitor H89 abrogated the $PGE_2$-induced expression of COX-2, suggesting involvement of the MAPK and PKA pathways. These results demonstrate that $PGE_2$ signaling acts in an autocrine manner, and specific inhibition of $PGE_2$ will provide a novel approach for the treatment of leukemia.

• 한국발생생물학회지:발생과생식
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• 제24권1호
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• pp.53-62
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• 2020

Natural killer (NK) cells are innate lymphocytes that play an essential role in preventing cancer development by performing immune surveillance to eradicate abnormal cells. Since ex vivo expanded NK cells have cytotoxic activity against various cancers, including breast cancers, their clinical potential as immune-oncogenic therapeutics has been widely investigated. Here, we report that the pyrazole chemical XRP44X, an inhibitor of Ras/ERK activation of ELK3, stimulates NK-92MI cells to enhance cytotoxic activity against breast cancer cells. Under XRP44X stimulation, NK cells did not show notable apoptosis or impaired cell cycle progression. We demonstrated that XRP44X enhanced interferon gamma expression in NK-92MI cells. We also elucidated that potentiation of the cytotoxic activity of NK-92MI cells by XRP44X is induced by activation of the c-JUN N-terminal kinase (JNK) signaling pathway. Our data provide insight into the evaluation of XRP44X as an immune stimulant and that XRP44X is a potential candidate compound for the therapeutic development of NK cells.

• Asian Pacific Journal of Cancer Prevention
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• 제16권6호
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• pp.2459-2463
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• 2015

Background: To investigate the expression and clinical significance of zinc finger protein 217 (ZNF217) in human colorectal carcinoma (CRC). Materials and Methods: The expression of ZNF217 in 60 CRC tissues and matched tumor adjacent tissues, collected between January 2013 and June 2014, was assessed immunohistochemically. The relationship between the expression of ZNF217 and clinicopathlogical features was analyzed by Pearson chi-square test. In addition, siRNA was used to down-regulate the expression of ZNF217 in CRC cells. The effects of ZNF217 for cell migration and invasion were measured by wound healing assay and transwell assay, respectively. Results: The expression level of ZNF217 was significantly higher in CRC tissues than in tumor adjacent tissues (p<0.05), positively correlating with tumor size, lymphatic metastasis and advanced TNM stage (p<0.05). Down-regulation of ZNF217 in CRC cells could significantly suppress cell migration and invasion. Conclusions: ZNF217 is overexpressed in colorectal carcinoma tissues and is associated with tumor malignant clinicopathological features. ZNF217 may promote CRC progression by inducing cell migration and invasion.

• Asian Pacific Journal of Cancer Prevention
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• 제15권23호
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• pp.10181-10185
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• 2015

Background: MicroRNAs, small noncoding RNA molecules, can regulate mammalian cell growth, apoptosis and differentiation by controlling the expression of target genes. The aim of this study was to investigate the function of miR-323-5p in the glioma cell line, U251. Materials and Methods: After over-expression of miR-323-5p using miR-323-5p mimics, cell growth, apoptosis and migration were tested by MTT, flow cytometry and cell wound healing assay, respectively. We also assessed the influence of miR-323-5p on the mRNA expression of IGF-1R by quantitative real-time reverse transcriptase PCR (qRT-PCR), and on the protein levels by Western blot analysi. In addition, dual-luciferase reporter assays were performed to determine the target site of miR-323-5p to IGF-1R 3'UTR. Results: Our findings showed that over-expression of miR-323-5p could promote apoptosis of U251 and inhibit the proliferation and migration of the glioma cells. Conclusions: This study demonstrated that increased expression of miR-323-5p might be related to glioma progression, which indicates a potential role of miR-323-5p for clinical therapy.

• Asian Pacific Journal of Cancer Prevention
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• 제13권6호
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• pp.2563-2569
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• 2012

Oxidative stress is a common mechanism contributing to initiation and progression of hepatic damage in a variety of liver disorders. Hence there is a great demand for the development of agents with potent antioxidant effect. The aim of the present investigation is to evaluate the efficacy of Moringa oleifera as a hepatoprotective and an antioxidant against 7, 12-dimethylbenz[a]anthracene induced hepatocellular damage. Single oral administration of DMBA (15 mg/kg) to mice resulted in significantly (p<0.001) depleted levels of xenobiotic enzymes like, cytochrome P450 and b5. DMBA induced oxidative stress was confirmed by decreased levels of reduced glutathione (GSH) and glutathione-S-transferase (GST) in the liver tissue. The status of hepatic aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP) which is indicative of hepatocellular damage were also found to be decreased in DMBA administered mice. Pretreatment with the Moringa oleifera (200 and 400 mg/kg) orally for 14 days significantly reversed the DMBA induced alterations in the liver tissue and offered almost complete protection. The results from the present study indicate that Moringa oleifera exhibits good hepatoprotective and antioxidant potential against DMBA induced hepatocellular damage in mice that might be due to decreased free radical generation.

• Asian Pacific Journal of Cancer Prevention
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• 제16권11호
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• pp.4509-4513
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• 2015

Osteosarcoma is the most common primary bone tumor in humans, especially in childhood. However, the genetic etiology for its pathogenesis remains elusive. It is known that microRNAs (miRNAs) are involved in the development of tumor progression. Here we show that microRNA-9 (miR-9) is a potential oncogene upregulated in osteosarcoma cells. Knockdown of miR-9 in osteosarcoma resulted in suppressed colony formation and cell proliferation. Further study identified GCIP, a Grap2 and cyclin D interacting protein, as a direct target of miR-9. In addition, GCIP overexpression activated retinoblastoma 1 (Rb) and suppressed E2F transcriptional target expression in osteosarcoma cells. Moreover, GCIP depletion reversed miR-9 knockdown induced colony formation and cell proliferation suppression. In sum, these results highlight the importance of miR-9 as an oncogene in regulating the proliferation of osteosarcoma by directly targeting GCIP and may provide new insights into the pathogenesis of osteosarcoma.

• Asian Pacific Journal of Cancer Prevention
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• 제16권18호
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• pp.8085-8091
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• 2016

Human papillomavirus is a virus that is distributed worldwide, and persistent infection with high-risk genotypes (HR-HPV) is considered the most important factor for the development of squamous cell cervical carcinoma (SCC). However, by itself, it is not sufficient, and other factors may contribute to the onset and progression of lesions. For example, infection with other sexually transmitted diseases such as human immunodeficiency virus (HIV) may be a factor. Previous studies have shown the relationship between HPV infection and SCC development among HIV-infected women in many regions of the world, with great emphasis on low- and middle-income countries (LMICs). Brazil is considered a LMIC and has great disparities across different regions. The purpose of this review was to highlight the current knowledge about HPV infection and cervical abnormalities in HIV+ women in Brazil because this country is an ideal setting to evaluate HIV impact on SCC development and serves as model of LMICs and low-resource settings.

• Asian Pacific Journal of Cancer Prevention
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• 제14권1호
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• pp.165-171
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• 2013

The aim of the present study was to analyze the expression of FHIT and WWOX in nasopharyngeal carcinoma (NPC) and correlations with clinical pathologic features. mRNA expression of the FHIT and WWOX was assessed by real-time fluorescent relatively quantitative PCR in 61 NPC tissues and 45 non-cancerous nasopharyngeal tissues. As a result, mRNA expression levels of both FHIT and WWOX were significantly lower in NPC patients than in control samples (P=0.049 and 0.045, respectively). Moreover, the mRNA expression of both had an inverse relation with larger invasive range (P=0.035 and 0.048, respectively), poor histologic differentiation (P=0.012 and 0.016) and advanced clinical stage (P=0.026 and 0.038). Consistency was found between expression of FHIT and WWOX in the same NPC tissues (r=0.681, P=0.00). In conclusion, synergy between FHIT and WWOX may exist in the development of NPC so that the two factors may be considered as important genetic markers. Detecting the expression of FHIT and WWOX should provide clinically significant information relevatn to tumor diagnosis, progression and treatment modalities for NPC.

• Journal of Chest Surgery
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• 제32권2호
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• pp.151-157
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• 1999

배경: 많은 실험적인 연구에서 종양 조직 내의 아포프토시스와 미세 혈관의 생성은 서로 반비례한다고 보고된다. 비소세포 폐암 조직내에서 두 수치의 관계를 조사하여 보았다. 대상 및 방법:조직내의 아포프토시스의 정도는 deoxynucleotidyl trasferase방법으로(Apop Tag In Situ Apoptosis Detection Kit, ONCOR) 측정하였고, 종양내 미세 혈관 밀도는 항 CD 31 항체를 이용하였다. 결과:아포프토시스 지수와 종양내 미세 혈관 밀도 사이에는 통계적으로 유의하게 역 상관관계가 있었다(p = 0.047). 결론: 비소세포 폐암종에서 아포프토시스와 미세 혈관 생성의 정도는 서로 연관이 있다고에 할 수있다. 그리고 종양내의 신생 혈관의 생성이 종양내 아포프토시스의 억제에 기여한다고 유추 할 수 있다.