网站标志
当前日期时间
当前时间:
点评详情
发布于:2019-6-13 09:39:08  访问:6 次 回复:0 篇
版主管理 | 推荐 | 删除 | 删除并扣分
Of miR-21 has been observed in association with UV-irradiation as well as other
MiR-21 signaling of IndigoAutophagy melanoma cells can be upregulated by exosomal transfer of miR-21. Moreover, inhibition of miR-21 increases chemosensitivity in a selection of tumors [220?23]. There is certainly additional proof that anti-miR-21 remedy downregulates the anti-apoptotic mitochondrial membrane protein BCL2 (B-cell PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28499442 leukemia two), which blocks apoptotic cell death [251]. BCL2 can be a MITF target gene involved in melanocyte and melanoma cell proliferation and survival [252, 253]. Combined inhibition of NF-B and BCL2 triggers synergistic reduction of viability and induces apoptosis in melanoma cells [254]. Remarkably, miR-21 inhibition suppresses proliferation and migration of nasopharyngeal carcinoma and breast cancer cells by means of downregulation of anti-apoptotic BCL2 [255, 256]. Furthermore, disruption of miR-21 by transcription activator-like effector nucleases (TALENs) in cancerous cells result in diminished cell transformation and elevated expression of cell-environment interaction genes [257]. Taken collectively, melanoma is usually a model cancer technique not merely involving genetic but also environmental elements [258]. At the molecular level, miR-21 links environmental exposure to melanomagenesis. Circulating exosomal miRs, specially miR-21, represents an incredibly important signaling program of cell communication [259] that apparently mediates the effect of environmentaland epigenetic factors in melanomagenesis. Circulating and locally generating exosomal miR-21 by means of many environmental stimuli may well considerably contribute for the multistep procedure of melanomagenesis. Decreasing the input and magnitude of extrinsic and intrinsic stimuli that promote ove.Of miR-21 has been observed in association with UV-irradiation and also other electromagnetic radiation, smoking, pollution with exposure to particulate matter and diesel exhaust. MiR-21 signaling of melanoma cells may be upregulated by exosomal transfer of miR-21. Exosomes have already been identified as key players sustaining a molecular crosstalk in between tumor cells andMelnik. J Transl Med (2015) 13:Web page 10 ofcell in the innate immune program [246]. Exosomes may possibly reach pigmented lesions either by way of bystander effects of UV-irradiated keratinocytes or by means of the circulation or underlying subcutaneous adipose tissue in obesity. As a result, environmental and intrinsic variables may well operate in an additive or synergistic manner, thereby growing the total person burden of miR-21 signaling (Figure 3). It is actually of special concern that miR-21 not merely promotes melanoma progression, but that it is also involved within the initiation of melanoma. MiR-21-mediated suppression of MSH2-dependent DNA mismatch repair, insufficient FoxO-controlled ROS-homeostasis, imbalances of FBXO11-regulated proteasomal degradation of crucial proteins involved in cell proliferation and apoptosis, and miR-21-stimulated telomerase activity may well all improve genetic instability advertising the danger of mutagenesis. Within this regard, miR-21 may well represent the prevalent denominator of accumulating environmental and intrinsic stressors that drive the initiation and progression of malignant melanoma PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27906190 (Figure three). The versatility of miRs as molecular tools inspires the design of novel techniques for the remedy of malignant melanoma [247]. As recommended for glioblastoma and ovarian carcinoma [248, 249], anti-miR-21 remedy could be a promising choice for the remedy of malignant melanoma [79]. It has been demonstrated that the curcumin analog EF24 exhibited potent anticancer activity in B16 murine melanoma cells linked having a downregulation of miR-21 [250].
共0篇回复 每页10篇 页次:1/1
共0篇回复 每页10篇 页次:1/1
我要回复
回复内容
验 证 码
看不清?更换一张
匿名发表 
会员登录
登录账号:
登录密码:
验 证 码:
您好,您已登录
您有条新到站内短信
会员中心 退出登录
 
 
脚注信息

版权所有 Copyright @ 2018-2020  三晋新闻网 提供

点击收缩

在线客服

    返回顶部