• 제목/요약/키워드: Micro-Targeting

검색결과 132건 처리시간 0.021초

다발성골수종 환자의 파라핀포매조직에서 MicroRNA 발현 (Expression of Micro RNA in Paraffin Embedded Tissue of Multiple Myeloma)

  • 최우순;권계철
    • 대한임상검사과학회지
    • /
    • 제47권4호
    • /
    • pp.292-297
    • /
    • 2015
  • 우리나라의 경우 갑상선암, 간암, 폐암 관련 연구가 보고되었으나 다발성 골수종환자에 관한 microRNA 연구는 보고된 경우가 없어 알아보고자 하였다. 또한, 다발성 골수종 환자의 골수(bone marrow)에서 채취한 검체를 이용한 연구가 대부분 보고되고 있으며, 파라핀 포매 조직을 이용한 경우는 거의 없어 파라핀 포매 조직에서도 가능한지 알아보았다. 연구 대상은 2010년 1월부터 2012년 7월까지 충남대학교병원 진단검사의학과에 다발성 골수종 진단을 위해 골수검사를 의뢰한 8 검체를 대상으로 하였다. microRNA는 보고된 내용 중 관련성이 높다고 한 miR-15a와 miR-16, miR-21, miR-181a, miR-221를 시행하여 다음과 같은 결과를 얻었다. 각 검체별 fold change 값이 1.5 이상 또는 -1.5 이하로 유의성을 보인 경우는 miR-15a에서 3예(37.5%)로 나타났다. Microarray 검사법으로 보고한 기존 연구와 비교한 결과, miR-15a의 경우 일치하는 결과로 한국인의 다발성 골수종 환자에서 진단에 활용할 수 있음을 확인하였다. miR-221은 상반된 결과를 얻었다. 이와 같이 miR-15a의 경우, 서양인과 일치하는 결과를 얻었으며, miR-221은 서양인과 상반된 결과로 좀 더 연구가 필요하리라 생각된다. 파라핀 포매 조직에서도 microRNA를 검출 할 수 있음을 확인하였다. 하지만 검체수가 적어 좀 더 정확한 확인 검사와 많은 검체를 이용한 연구가 더욱 필요하다.

Ginsenosides: potential therapeutic source for fibrosis-associated human diseases

  • Li, Xiaobing;Mo, Nan;Li, Zhenzhen
    • Journal of Ginseng Research
    • /
    • 제44권3호
    • /
    • pp.386-398
    • /
    • 2020
  • Tissue fibrosis is an eventual pathologic change of numerous chronic illnesses, which is characterized by resident fibroblasts differentiation into myofibroblasts during inflammation, coupled with excessive extracellular matrix deposition in tissues, ultimately leading to failure of normal organ function. Now, there are many mechanistic insights into the pathogenesis of tissue fibrosis, which facilitate the discovery of effective antifibrotic drugs. Moreover, many chronic diseases remain a significant clinical unmet need. For the past five years, many research works have undoubtedly addressed the functional dependency of ginsenosides in different types of fibrosis and the successful remission in various animal models treated with ginsenosides. Caveolin-1, interleukin, thrombospondin-1 (TSP-1), liver X receptors (LXRs), Nrf2, microRNA-27b, PPARδ-STAT3, liver kinase B1 (LKB1)-AMPK, and TGF-β1/Smads are potential therapy targeting using ginsenosides. Ginsenosides can play a targeting role and suppress chronic inflammatory response, collagen deposition, and epitheliale-mesenchymal transition (EMT), as well as myofibroblast activation to attenuate fibrosis. In this report, our aim was to focus on the therapeutic prospects of ginsenosides in fibrosis-related human diseases making use of results acquired from various animal models. These findings should provide important therapeutic clues and strategies for the exploration of new drugs for fibrosis treatment.

miR-124 Inhibits Growth and Invasion of Gastric Cancer by Targeting ROCK1

  • Hu, Cong-Bing;Li, Qiao-Lin;Hu, Jian-Fei;Zhang, Qiang;Xie, Jian-Ping;Deng, Li
    • Asian Pacific Journal of Cancer Prevention
    • /
    • 제15권16호
    • /
    • pp.6543-6546
    • /
    • 2014
  • MicroRNAs (miRNAs) act as critical regulators of genes involved in many biological processes. Aberrant alteration of miRNAs have been found in many cancers, including gastric cancer (GC), but the molecular mechanisms are not well understood. Herein, we investigated the role of miR-124 in GC. We found that its expression was significantly reduced in both GC tissue samples and cell lines. Forced expression of miR-124 suppressed GC cell proliferation, migration, and invasion. Furthermore, the Rho-associated protein kinase (ROCK1) was identified as a direct target of miR-124 in GC cells. Finally, silencing of ROCK1 showed similar effects as miR-124 overexpression, while supplementation of ROCK1 remarkably restored the cell growth and invasion inhibited by miR-124. Together, our data demonstrate that miR-124 acts as a tumor suppressor by targeting ROCK1, and posit miR-124 as a novel strategy for GC treatment.

miR-29a suppresses growth and invasion of gastric cancer cells in vitro by targeting VEGF-A

  • Chen, Ling;Xiao, Hong;Wang, Zong-Hua;Huang, Yi;Liu, Zi-Peng;Ren, Hui;Song, Hang
    • BMB Reports
    • /
    • 제47권1호
    • /
    • pp.39-44
    • /
    • 2014
  • Increasing data shows miR-29a is a key regulator of oncogenic processes. It is significantly down-regulated in some kind of human tumors and possibly functionally linked to cellular proliferation, survival and migration. However, the mechanism remains unclear. In this study, we report miR-29a is significantly under-expressed in gastric cancer compared to the healthy donor. The microvessel density is negatively related to miR-29a expression in gastric cancer tissues. The ectopic expression of miR-29a significantly inhibits proliferation and invasion of gastric cancer cells. Furthermore, western blot combined with the luciferase reporter assays demonstrate that vascular endothelial growth factor A (VEGF-A) is direct target of miR-29a. This is the first time miR-29a was found to suppress the tumor microvessel density in gastric cancer by targeting VEGF-A. Taken together, these results suggest that miR-29a is a tumor suppressor in gastric cancer. Restoration of miR-29a in gastric cancer may be a promising therapeutic approach.

Inhibition of Cell Proliferation and Migration by miR-509-3p That Targets CDK2, Rac1, and PIK3C2A

  • Yoon, Sena;Han, Eunji;Choi, Young-Chul;Kee, Honghwan;Jeong, Yongsu;Yoon, Jaeseung;Baek, Kwanghee
    • Molecules and Cells
    • /
    • 제37권4호
    • /
    • pp.314-321
    • /
    • 2014
  • CDK2 is a key regulator of cell cycle progression. In this study, we screened for miRNAs targeting CDK2 using a luciferase-3'-untranslated region reporter assay. Among 11 hit miRNAs, miR-509-3p reduced CDK2 protein levels and significantly inhibited cancer cell growth. Microarray, Western blotting, and luciferase reporter analyses revealed additional targets of miR-509-3p, including Rac1 and PIK3C2A. Overexpression of miR-509-3p induced G1 cell-cycle arrest and inhibited colony formation and migration. RNAi experiments indicated that the growth-inhibitory effects of miR-509-3p may occur through down-regulation of CDK2, Rac1, and PIK3C2A. Targeting of multiple growth regulatory genes by miR-509-3p may contribute to effective anti-cancer therapy.

DSP 기반 초소형 수중 음향통신 모뎀 (DSP-Based Micro-Modem for Underwater Acoustic Communications)

  • 이동수;이상민;박성준
    • 한국통신학회논문지
    • /
    • 제39C권3호
    • /
    • pp.275-281
    • /
    • 2014
  • 최근 들어 연근해와 내수면에서 수중 자원의 효과적 개발과 보존을 위해 다양한 수중 응용 시스템 발굴 및 활용의 필요성이 증대되고 있다. 이에 본 논문에서는 근거리 수중 이동통신 시스템, 수중 센서네트워크 시스템 등의 핵심 기술 중의 하나인 초소형 수중 음향통신 모뎀의 디지털 모듈을 연구한다. 고속 연산처리가 가능한 디지털 신호처리 프로세서를 탑재한 수중 모뎀의 디지털 모듈을 설계하고 제작하며, 개발된 하드웨어에 프레임 형성 기능과 채널부호 알고리듬들을 구현하고 실험함으로써 회로의 기능과 성능을 검증한다. 실험 결과에 따르면, 개발된 DSP 기반 디지털 모듈에서 전송속도 1 kbps의 길쌈부호 처리를 위해 필요로 하는 연산량이 DSP의 가용 연산 능력의 1% 이내에 불과하므로 개발된 하드웨어 플랫폼에 다양한 고효율 기저대역 알고리듬을 탑재함으로써 수중 모뎀의 성능 개선을 모색할 수 있다.

Global and Local Competition between Exogenously Introduced microRNAs and Endogenously Expressed microRNAs

  • Kim, Doyeon;Kim, Jongkyu;Baek, Daehyun
    • Molecules and Cells
    • /
    • 제37권5호
    • /
    • pp.412-417
    • /
    • 2014
  • It has been reported that exogenously introduced micro-RNA (exo-miRNA) competes with endogenously expressed miRNAs (endo-miRNAs) in human cells, resulting in a detectable upregulation of mRNAs with endo-miRNA target sites (TSs). However, the detailed mechanisms of the competition between exo- and endo-miRNAs remain uninvestigated. In this study, using 74 microarrays that monitored the whole-transcriptome response after introducing miRNAs or siRNAs into HeLa cells, we systematically examined the derepression of mRNAs with exo- and/or endo-miRNA TSs. We quantitatively assessed the effect of the number of endo-miRNA TSs on the degree of mRNA derepression. As a result, we observed that the number of endo-miRNA TSs was significantly associated with the degree of derepression, supporting that the derepression resulted from the competition between exo- and endo-miRNAs. However, when we examined whether the site proficiency of exo-miRNA TSs could also influence mRNA derepression, to our surprise, we discovered a strong positive correlation. Our analysis indicates that site proficiencies of both exo- and endo-miRNA TSs are important determinants for the degree of mRNA derepression, implying that the derepression of mRNAs in response to exo-miRNA is more complex than that currently perceived. Our observations may lead to a more complete understanding of the detailed mechanisms of the competition between exo- and endo-miRNAs and to a more accurate prediction of miRNA targets. Our analysis also suggests an interesting hypothesis that long 3'-UTRs may function as molecular buffer against gene expression regulation by individual miRNAs.

MicroRNA 449c Mediates the Generation of Monocytic Myeloid-Derived Suppressor Cells by Targeting STAT6

  • Han, Xiaoqing;Luan, Tao;Sun, Yingying;Yan, Wenyi;Wang, Dake;Zeng, Xianlu
    • Molecules and Cells
    • /
    • 제43권9호
    • /
    • pp.793-803
    • /
    • 2020
  • Myeloid-derived suppressor cells (MDSCs) promote tumour progression by contributing to angiogenesis, immunosuppression, and immunotherapy resistance. Although recent studies have shown that microRNAs (miRNAs) can promote the expansion of MDSCs in the tumour environment, the mechanisms involved in this process are largely unknown. Here, we report that microRNA 449c (miR-449c) expression was upregulated in myeloid progenitor cells upon activation of C-X-C motif chemokine receptor 2 (CXCR2) under tumour conditions. MiR-449c upregulation increased the generation of monocytic MDSCs (mo-MDSCs). The increased expression of miR-449c could target STAT6 mRNA in myeloid progenitor cells to shift the differentiation balance of myeloid progenitor cells and lead to an enhancement of the mo-MDSCs population in the tumour environment. Thus, our results demonstrate that the miR-449c/STAT6 axis is involved in the expansion of mo-MDSCs from myeloid progenitor cells upon activation of CXCR2, and thus, inhibition of miR-449c/STAT6 signalling may help to attenuate tumour progression.

한반도 중서부 도서지역에 있어서 사면 미지형과 옛 주거지 분포와의 대응관계 (A Relationship between Micro-Landforms and Distribution of the Ancient Dwelling Site in the Middle Western area, Korea)

  • 박지훈;최성길
    • 한국지형학회지
    • /
    • 제20권3호
    • /
    • pp.109-118
    • /
    • 2013
  • 본 연구목적은 지형학적 관점에서 한반도 중서부 도서지역인 인천 영종도에 있어서 신석기 및 청동기시대 주거지의 최적 입지환경을 밝히는 것이다. 이를 위하여 현재까지 조사지역에서 확인된 주거지들 중에서 정량분석이 가능한 신석기시대와 청동기시대 주거지 각각 145기와 47기를 대상으로 개별 주거지들의 미지형 입지환경을 분석하였다. 그 결과, 신석기 및 청동기시대 주거지가 가장 많이 밀집하는 구릉의 미지형은 각각 상부곡벽사면(64기, 44.1%)과 정부사면(39기, 83%)인 것으로 판명되었다. 이것은 지형학적 관점에서 볼 때, 조사지역의 경우, 신석기시대에서 청동기시대로 가면서 주거지 최적 입지환경이 바뀌었으며 주거지가 입지하는 구릉의 미지형의 위치도 상대적으로 약간 상승했다는 것을 의미한다.

MicroRNA-576-3p Inhibits Proliferation in Bladder Cancer Cells by Targeting Cyclin D1

  • Liang, Zhen;Li, Shiqi;Xu, Xin;Xu, Xianglai;Wang, Xiao;Wu, Jian;Zhu, Yi;Hu, Zhenghui;Lin, Yiwei;Mao, Yeqing;Chen, Hong;Luo, Jindan;Liu, Ben;Zheng, Xiangyi;Xie, Liping
    • Molecules and Cells
    • /
    • 제38권2호
    • /
    • pp.130-137
    • /
    • 2015
  • MicroRNAs (miRNAs) are small, endogenous RNAs that play important gene-regulatory roles by binding to the imperfectly complementary sequences at the 3'-UTR of mRNAs and directing their gene expression. Here, we first discovered that miR-576-3p was down-regulated in human bladder cancer cell lines compared with the non-malignant cell line. To better characterize the role of miR-576-3p in bladder cancer cells, we over-expressed or down-regulated miR-576-3p in bladder cancer cells by transfecting with chemically synthesized mimic or inhibitor. The overexpression of miR-576-3p remarkably inhibited cell proliferation via G1-phase arrest, and decreased both mRNA and protein levels of cyclin D1 which played a key role in G1/S phase transition. The knock-down of miR-576-3p significantly promoted the proliferation of bladder cancer cells by accelerating the progression of cell cycle and increased the expression of cyclin D1. Moreover, the dual-luciferase reporter assays indicated that miR-576-3p could directly target cyclin D1 through binding its 3'-UTR. All the results demonstrated that miR-576-3p might be a novel suppressor of bladder cancer cell proliferation through targeting cyclin D1.