• 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.

• 한국지구물리탐사학회:학술대회논문집
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• 한국지구물리탐사학회 2008년도 공동학술대회
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• pp.51-56
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• 2008

등방성 매질에서의 파형역산에 대한 연구는 1980년대부터 꾸준히 이루어져 왔으나 이방성 매질에 대한 연구는 그렇지 못하다. 본 연구에서는 이방성 매질에 대한 시간영역 셀기반 유한 차분 모델링 기법을 이용해 2차원 TI 구조에서의 파형역산 알고리듬을 개발하였다. 반복적인 비선형 역산에서 최대 급경사 방향은 역시간 구조보정의 역전파 방법을 이용하여 간접적으로 계산하였고, 이를 정규화 시키기 위해 슈도-헤시안 행렬을 이용하였다. 본 연구에서 제시된 시간영역 파형역산 기법을 이방성 매질을 포함한 2층 구조와 이방성 Marmousi 모형 자료에 적용하고 이를 등방성 매질만을 고려한 기존의 파형역산 결과와 비교하였다. 본 연구의 결과를 통해 이방성 매질을 등방성 매질로 가정하고 파형역산을 수행할 경우 정확한 영상을 얻을 수 없기 때문에, 실제 탐사 자료의 파형역산을 수행할 경우 이방성 매질을 고려해야 좀 더 정확한 지하 구조를 파악할 수 있음을 확인하였다.

• 지구물리와물리탐사
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• 제11권3호
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• pp.177-183
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• 2008

석유탐사 분야에서 탐사대상이 되는 저류층이 갈수록 심부화되고 복잡한 지층 구조로 옮겨감에 따라 암염층 하부 구조를 영상화하는 기술은 석유 및 가스층의 탐지를 위해 매우 중요하게 부각되고 있다. 그러나 암염돔 구조의 특성상 안염돔 하부로부터의 반사 에너지가 미약하기 때문에 하부구조의 정확한 영상을 얻기는 힘들다. 이러한 어려움을 극복하고자 본 연구에서는 암염돔 하부 구조 영상화를 위해 다중격자(multi-grid) 기법을 사용하여 파형역산을 수행하였다. 고정격자를 이용한 통상적인 주파수 영역 파형역산 기법으로 얻은 결과와의 비교를 통해 암염돔 구조 및 하부 구조의 영상화에서 다중격자를 적용한 파형역산 기법의 장점을 확인하였다. 본 연구 결과를 통해 고정격자를 이용한 파형역산 기법으로 정확한 영상을 얻기 어려웠던 암염돔 구조에서도 다중격자를 적용하여 향상된 영상을 얻을 수 있음을 보여 주었다.

• Asian Pacific Journal of Cancer Prevention
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• 제14권1호
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• pp.173-177
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• 2013

Backgrounds: Tanshinone IIA (TIIA), a phenanthrenequinone derivative extracted from Salvia miltiorrhiza BUNGE, has been reported to be a natural anti-cancer agent in a variety of tumor cells. However, the effect of TIIA on gastric cancer cells remains unknown. In the present study, we investigated the influence of TIIA on the malignant phenotype of SGC7901 gastric cancer cells. Methods: Cells cultured in vitro were treated with TIIA (0, 1, 5, $10{\mu}g/ml$) and after incubation for different periods, cell proliferation was measured by MTT method and cell apoptosis and cell cycling were assessed by flow cytometry (FCM). The sensitivity of SGC7901 gastric cancer cells to anticancer chemotherapy was investigated with the MTT method, while cell migration and invasion were examined by wound-healing and transwell assays, respectively. Results: TIIA (1, 5, $10{\mu}g/ml$) exerted powerful inhibitory effects on cell proliferation (P < 0.05, and P < 0.01), and this effect was time- and dose-dependent. FCM results showed that TIIA induced apoptosis of SGC7901 cells, reduced the number of cells in S phase and increased those in G0/G1 phase. TIIA also significantly increased the sensitivity of SGC7901 gastric cancer cells to ADR and Fu. Moreover, wound-healing and transwell assays showed that TIIA markedly decreased migratory and invasive abilities of SGC7901 cells. Conclusions: TIIA can reverse the malignant phenotype of SGC7901 gastric cancer cells, indicating that it may be a promising therapeutic agent.

• Molecules and Cells
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• 제41권6호
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• pp.591-602
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• 2018

Gastric cancer is the fifth most common type of malignancy worldwide, and the survival rate of patients with advanced-stage gastric cancer is low, even after receiving chemotherapy. Here, we validated neurotensin receptor 1 (NTSR1) as a potential therapeutic target in gastric cancer. We compared NTSR1 expression levels in sixty different gastric cancer-tissue samples and cells, as well as in other cancer cells (lung, breast, pancreatic, and colon), by assessing NTSR1 expression via semi-quantitative real-time reverse transcription polymerase chain reaction, immunocytochemistry and western blot. Following neurotensin (NT) treatment, we analyzed the expression and activity of matrix metalloproteinase-9 (MMP-9) and further determined the effects on cell migration and invasion via wound-healing and transwell assays. Our results revealed that NTSR1 mRNA levels were higher in gastric cancer tissues than non-cancerous tissues. Both of NTSR1 mRNA levels and expression were higher in gastric cancer cell lines relative to levels observed in other cancer-cell lines. Moreover, NT treatment induced MMP-9 expression and activity in all cancer cell lines, which was significantly decreased following treatment with the NTSR1 antagonist SR48692 or small-interfering RNA targeting NTSR1. Furthermore, NT-mediated metastases was confirmed by observing epithelial-mesenchymal transition markers SNAIL and E-cadherin in gastric cancer cells. NT-mediated invasion and migration of gastric cancer cells were reduced by NTSR1 depletion through the Erk signaling. These findings strongly suggested that NTR1 constitutes a potential therapeutic target for the inhibition of gastric cancer invasion and metastasis.

• Journal of Ginseng Research
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• 제43권1호
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• pp.68-76
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• 2019

Background: In colorectal cancer (CRC), 40-60% of patients develop metastasis. The epithelial-mesenchymal transition (EMT) is a pivotal and intricate process that increases the metastatic potential of CRC. The aim of this study was to investigate the effect of Korean Red Ginseng extract (RGE) on colorectal metastasis through inhibition of EMT and the metastatic abilities of CRC cells. Methods: To investigate the effect of RGE on the metastatic phenotypes of CRC cells, CT26 and HT29 cells were evaluated by using an adhesion assay, a wound-healing assay, an invasion assay, zymography, and real-time reverse transcription-polymerase chain reaction. Western-blot analysis was conducted to elucidate the molecular mechanisms of RGE, which showed an inhibitory effect on the transforming growth factor-${\beta}1$ ($TGF-{\beta}1$)-induced EMT in HT29 cells. Additionally, the antimetastatic effect of RGE was evaluated in a mouse model of lung metastasis injected with CT26 cells. Results: RGE decreased the adhesion and migration ability of the CT26 cells and TGF-${\beta}1$-treated HT29 cells. The invasion ability was also reduced by RGE treatment through the inhibition of matrix metalloproteinase-9 expression and activity. Moreover, RGE suppressed the TGF-${\beta}1$-induced EMT via TGF-${\beta}1$/Smad-signaling-mediated Snail/E-cadherin expression in HT29 cells and lung tissue in CT26 tumor-bearing mice. Conclusion: Our results demonstrated that RGE inhibited colorectal lung metastasis through a reduction in metastatic phenotypes, such as migration, invasion, and the EMT of CRC cells.

• Journal of Microbiology and Biotechnology
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• 제32권10호
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• pp.1344-1354
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• 2022

Laryngeal cancer is one of the highest incidence, most prevalently diagnosed head and neck cancers, making it critically necessary to probe effective targets for laryngeal cancer treatment. Here, real-time quantitative reverse transcription PCR (qRT-PCR) and western blot analysis were used to detect gene expression levels in laryngeal cancer cell lines. Fluorescence in situ hybridization (FISH) and subcellular fractionation assays were used to detect the subcellular location. Functional assays encompassing Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), transwell and wound healing assays were performed to examine the effects of target genes on cell proliferation and migration in laryngeal cancer. The in vivo effects were proved by animal experiments. RNA-binding protein immunoprecipitation (RIP), RNA pulldown and luciferase reporter assays were used to investigate the underlying regulatory mechanisms. The results showed that KIF26B antisense RNA 1 (KIF26B-AS1) propels cell proliferation and migration in laryngeal cancer and regulates the toll-like receptor 4 (TLR4) signaling pathway. KIF26B-AS1 also recruits FUS to stabilize TLR4 mRNA, consequently activating the TLR4 signaling pathway. Furthermore, KIF26B-AS1 plays an oncogenic role in laryngeal cancer via upregulating TLR4 expression as well as the FUS/TLR4 pathway axis, findings which offer novel insight for targeted therapies in the treatment of laryngeal cancer patients.

• Asian Pacific Journal of Cancer Prevention
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• 제14권10호
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• pp.5915-5920
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• 2013

Aim: Although aberrant miRNA expression has been documented, altered miR-101 expression in cervical cancer and its carcinogenic effects and mechanisms remain unexplored. The aim of our study was to investigate the role of miR-101 alteration in cervical carcinogenesis. Methods: Expression of miR-101 was examined by quantitative real-time reverse transcriptase PCR (qRT-PCR) in Hela cells. After modulating miR-101 expression using miR-101 mimics, cell growth, apoptosis and proliferation, and migration were tested separately by MTT or flow cytometry and cell wound healing assay and protein expression was detected by qRT-PCR. The expression of COX-2 in Hela cell was also examined by immunohistochemical staining and the correlation with miR-101 expression was analysed. Results: The miR-101 demonstrated significantly low expression in Hela cell. When we transfected miR-101 mimics into Hela cells, the modulation of miR-101 expression remarkably influenced cell proliferation, cycling and apoptosis: 1) The expression of microRNA-101 tended to increase after transfection; 2) Overexpression of miR-101 was able to promote cell apoptosis, the apoptosis rate being markedly higher (97.6%) than that seen pre-transfection (12.2%) (P<0.05); 3) The miR-101 negatively regulates cell migration and invasion, scratch results being lower ($42.7um{\pm}2um$) than that observed pre-transfection ($181.4um{\pm}2um$); 4) miRNA-101 inhibits the proliferation of Hela cells as well as the level of COX-2 protein, which was negatively correlated with miR-101 expression. Conclusions: Overexpression of miR-101 has obvious inhibitory effects on cell proliferation, migration and invasion. Thus reduced miR-101 expression could participate in the development of cervical cancer at least partly through loss of inhibition of target gene COX-2, which probably occurs in a relative late phase of carcinogenesis. Our data suggest an important role of miR-101 in the molecular etiology of cancer and indicate potential application of miR-101 in cancer therapy.

• 지구물리와물리탐사
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• 제14권3호
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• pp.214-219
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• 2011

본 논문에서는 시간영역에서 분리된 잔여 파동장을 이용하여 주파수영역 파형역산을 수행하였다. 시간영역 잔여 파동장들을 절대값의 크기에 따라 정렬하여 분류하고, 이를 여러 개의 그룹으로 분리하였다. 분리된 잔여 파동장들은 각 그룹별로 목적함수의 경사 방향을 정규화한 후 평균하기 때문에 통상적인 잔여 파동장에서 작은 크기를 가지는 파동장들을 상대적으로 강조하는 효과가 있고, 이는 파형역산 시 심부구조의 이미지 향상에 도움을 준다. 파형역산은 시간영역에서 분리된 잔여 파동장을 이용하여 주파수영역에서 수행되며, 목적함수의 경사방향은 구조보정에서 많이 쓰이는 역전파 기법을 적용하여 계산된다. 본 연구에서 제안한 알고리듬의 타당성을 확인하기 위하여 SEG/EAGE 암염 모델과 Marmousi 모델을 이용하여 파형역산을 수행하였다. 역산 결과를 통해 제안된 알고리즘이 일반적인 주파수영역 파형역산에 비해 심부구조에 대하여 향상된 결과를 제시함을 확인하였다.

• 지구물리와물리탐사
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• 제20권3호
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• pp.129-136
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• 2017

파형 역산 또는 역시간 구조 보정과 같은 3차원 탄성파 자료 처리를 위해서는 3차원 파동 전파 모델링과 그에 따른 대량의 수치 계산이 필요하다. 본 연구에서는 3차원 주파수 영역 파동 전파 모델링을 이용해 제온 파이 가속기와 서버용 고성능 CPU의 성능 및 정확성을 비교하였다. 시간 영역 유한 차분법 알고리즘에 제온 파이의 특징을 고려하여 OpenMP 병렬 프로그래밍을 적용하였다. 주파수 영역 파동장을 얻기 위해서는 시간 영역 모델링과 동시에 푸리에 변환을 수행하였다. 3차원 SEG/EAGE 암염돔 속도 모델을 사용하여 주파수 영역 파동장을 생성한 결과, 제온 파이를 이용해 정확한 주파수 영역 파동장을 CPU 대비 1.44배 빠르게 얻을 수 있었다.