• 제목/요약/키워드: microRNA-204

검색결과 5건 처리시간 0.018초

MiR-204 acts as a potential therapeutic target in acute myeloid leukemia by increasing BIRC6-mediated apoptosis

  • Wang, Zhiguo;Luo, Hong;Fang, Zehui;Fan, Yanling;Liu, Xiaojuan;Zhang, Yujing;Rui, Shuping;Chen, Yafeng;Hong, Luojia;Gao, Jincheng;Zhang, Mei
    • BMB Reports
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    • 제51권9호
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    • pp.444-449
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    • 2018
  • Acute myeloid leukemia (AML) is one of the most common hematological malignancies all around the world. MicroRNAs have been determined to contribute various cancers initiation and progression, including AML. Although microRNA-204 (miR-204) exerts anti-tumor effects in several kinds of cancers, its function in AML remains unknown. In the present study, we assessed miR-204 expression in AML blood samples and cell lines. We also investigated the effects of miR-204 on cellular function of AML cells and the underlying mechanisms of the action of miR-204. Our results showed that miR-204 expression was significantly downregulated in AML tissues and cell lines. In addition, overexpression of miR-204 induced growth inhibition and apoptosis in AML cells, including AML5, HL-60, Kasumi-1 and U937 cells. Cell cycle analysis further confirmed an augmentation in theapoptotic subG1 population by miR-204 overexpression. Mechanistically, baculoviral inhibition of apoptosis protein repeat containing 6 (BIRC6) was identified as a direct target of miR-204. Enforcing miR-204 expression increased the luciferase activity and expression of BIRC6, as well as p53 and Bax expression. Moreover, restoration of BIRC6 reversed the pro-apoptotic effects of miR-204 overexpression in AML cells. Taken together, this study demonstrates that miR-204 causes AML cell apoptosis by targeting BIRC6, suggesting miR-204 may play an anti-carcinogenic role in AML and function as a novel biomarker and therapeutic target for the treatment of this disease.

한국인의 다발성골수종 환자에서 MicroRNA-221의 발현 (Expression of MicroRNA-221 in Korean Patients with Multiple Myeloma)

  • 최우순
    • 대한임상검사과학회지
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    • 제50권2호
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    • pp.197-204
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    • 2018
  • 다발성 골수종(MM)은 혈액 종양의 주요 사망 원인이다. 최근에 다발성 골수종 진단에 microRNA를 이용한 실험이 보고되고 있다. 이에 우리는 다발성 골수종 진단 마커로 miR-221을 이용 할 수 있는지 확인하고자 하였다. 본 연구는 다른 혈액학적 질환이 없는 다발성 골수종 환자 20명을 대상으로 하였다. MicroRNA 추출은 다발성 골수종 환자의 파라핀 포매 조직을 이용하였다. 우리는 다발성 골수종의 microRNA 표적 유전자로 miR-15a, miR-16, miR-21, miR-181a 그리고 miR-221을 선택하였다. 유의성 검정은 fold change 값을 기준으로 1.5이상 또는 -1.5 미만의 결과를 유의성이 있는 경우로 하였다. Fold change 값은 인간 유전자 SNORD43에 의해 표준화된 데이터를 기준으로 하였다. Fold change 값이 1.5 이상은 "overexpression", -1.5 미만의 값은 "underexpression"으로 정의되었다. miR-221의 65.0% (13/20)에서 "overexpression"으로 유의성이 있음을 확인하였고, 다발성 골수종 환자에서 형질세포가 30% 이상인 그룹과 이하의 그룹은 유의성을 보이지 않았다. MiR-221은 서구인과 같은 결과를 얻었으며, 다발성 골수종 환자에서 miR-221이 다발성 골수종 환자 진단에 매우 중요한 지표가 될 수 있을 것으로 생각된다. 결론적으로 miR-221은 한국인의 다발성 골수종 진단 또는 예후 지표로 활용할 수 있음을 확인하였다.

MicroRNA-27 Promotes Odontoblast Differentiation via Wnt1 Signaling

  • Cho, Ji-Ho;Kim, Su-Gwan;Park, Byung-Sun;Go, Dae-San;Park, Joo-Cheol;Kim, Do Kyung
    • International Journal of Oral Biology
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    • 제40권4호
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    • pp.197-204
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    • 2015
  • MicroRNA (miRNA, miR) is essential in regulating cell differentiation either by inhibiting mRNA translation or by inducing its degradation. However, the role of miRNA in odontoblastic cell differentiation is still unclear. In this study, we examined the molecular mechanism of miR-27-mediated regulation of odontoblast differentiation in MDPC-23 mouse odontoblastic cells derived from mouse dental papilla cells. The results of the present study demonstrated that the miR-27 expression increases significantly during MDPC-23 odontoblastic cell differentiation. Furthermore, miR-27 up-regulation promotes the differentiation of MDPC-23 cells and accelerates mineralization without cell proliferation. The over-expression of miR-27 significantly increased the expression levels of Wnt1 mRNA and protein. In addition, the results of target gene prediction revealed that Wnt1 mRNA has an miR-27 binding site in its 3'UTR, and is increased by miR-27. These results suggested that miR-27 promotes MDPC-23 odontoblastic cell differentiation by targeting Wnt1 signaling. Therefore, miR-27 is a critical odontoblastic differentiation molecular target for the development of miRNA based therapeutic agents in dental medicine.

Downregulated MicroRNA-133a in Gastric Juice as a Clinicopathological Biomarker for Gastric Cancer Screening

  • Shao, Juan;Fang, Peng-Hua;He, Biao;Guo, Li-Li;Shi, Ming-Yi;Zhu, Yan;Bo, Ping;Zhang, Zhen-Wen
    • Asian Pacific Journal of Cancer Prevention
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    • 제17권5호
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    • pp.2719-2722
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    • 2016
  • Circulatory miR-133a is a marker shared by several types of cancer. In this study we evaluated the feasibility of using miR-133a levels in gastric juice to screen for gastric cancer. A total of 204 samples of gastric juice and mucosa from gastric cancer, atrophic gastritis, gastric ulcer, superficial gastritis and healthy cases were collected by gastroscopy. The results showed that miR-133a levels in gastric juice and carcinoma tissues of patients with gastric cancer were significantly downregulated and positively correlated. Moreover, miR-133a in gastric juice has high operability, high reliability, high sensitivity, high specificity and relative stability, fit for clinical diagnosis of gastric cancer.

2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-Glucoside modulated human umbilical vein endothelial cells injury under oxidative stress

  • Guo, Yan;Fan, Wenxue;Cao, Shuyu;Xie, Yuefeng;Hong, Jiancong;Zhou, Huifen;Wan, Haitong;Jin, Bo
    • The Korean Journal of Physiology and Pharmacology
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    • 제24권6호
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    • pp.473-479
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    • 2020
  • Endothelial cell injury is a major contributor to cardiovascular diseases. The 2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-Glucoside (TSG) contributes to alleviate human umbilical vein endothelial cells (HUVECs) injury through mechanisms still know a little. This study aims to clarify the TSG effects on gene expression (mRNA and microRNA) related to oxidative stress and endoplasmic reticulum stress induced by H2O2 in HUVECs. We found that TSG significantly reduced the death rate of cells and increased intracellular superoxide dismutase activity. At qRT-PCR, experimental data showed that TSG significantly counteracted the expressions of miR-9-5p, miR-16, miR-21, miR-29b, miR-145-5p, and miR-204-5p. Besides, TSG prevented the expression of ATF6 and CHOP increasing. In contrast, TSG promoted the expression of E2F1. In conclusion, our results point to the obvious protective effect of TSG on HUVECs injury induced by H2O2, and the mechanism may through miR16/ATF6/ E2F1 signaling pathway.