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Expressions of Long Non-Coding RNAs in Carcinogenesis of Cervix: A Review
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作者 Shrestha Reshies Min-Min Yu 《Open Journal of Obstetrics and Gynecology》 2018年第2期130-145,共16页
Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides mostly transcribed by RNA which do not encode proteins. Previously, lncRNAs were considered transcriptional byproducts called “junk DNA” wit... Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides mostly transcribed by RNA which do not encode proteins. Previously, lncRNAs were considered transcriptional byproducts called “junk DNA” with no biological functions. There are many studies conducted on lncRNAs showing they are actively involved in regulation of epigenetic, transcriptional, and post-transcriptional events. Expressions of lncRNAs are more different in many malignant tumors than in benign tumors and normal tissue. Aberration of lncRNAs is responsible to promote or suppress tumorigenesis and cancer progression. Under different circumstances, lncRNAs exhibit their roles in carcinogenesis such as MALAT1 is responsible for intervening mRNA instability, HOTAIR, MALAT1, ANRIL, PVT1 links with miRNA and histonemodifying complexes, MEG3 associates with miRNA, CCAT2, MEG3, GAS5, UCA1 allies with c-Myc or P53 causing suppression of tumor or oncogenesis. Abnormal expressions of lncRNAs are noticed in gynecological cancers, such as cervical cancer, ovarian cancer, and endometrial cancer. Identification of cervical cancer associated lncRNAs is necessary to understand the molecular biogenesis of cancers. In this review, we summarized the foundation and function of the lncRNAs in terms of tumor progression, invasion, prognosis, apoptosis, metastasis, and chemo-resistance. This review will provide references to determine the clinical applications of lncRNAs as ideal diagnostic biomarkers or therapeutic targets in cervical cancers. 展开更多
关键词 lncRNAs long non-coding RNAS CERVICAL Cancer HPV HOTAIR MALAT-1 GAS5 MEG3 PVT1 HULC ANRIL CCHE1 CCAT2 UCA1
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血管软化丸抑制血管炎症反应防治动脉粥样硬化的分子机制 被引量:4
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作者 秦合伟 牛雨晴 +2 位作者 宋雪梅 王梦楠 孙孟艳 《实用医学杂志》 CAS 北大核心 2022年第15期1901-1907,共7页
目的观察中药复方血管软化丸防治动脉粥样硬化(atherosclerosis,AS)是否通过靶向调控长链非编码RNA-TGFB2-OT1、miR4459及其下游信号抑制炎症反应产生效果。方法建立AS模型,采用血管软化丸干预、以TGFB2-OT1 inhibitor作为阳性对照;干预... 目的观察中药复方血管软化丸防治动脉粥样硬化(atherosclerosis,AS)是否通过靶向调控长链非编码RNA-TGFB2-OT1、miR4459及其下游信号抑制炎症反应产生效果。方法建立AS模型,采用血管软化丸干预、以TGFB2-OT1 inhibitor作为阳性对照;干预8周后进行生化检测,HE染色观察主动脉病理改变,Real-time PCR法和Western blot法检测主动脉TGFB2-OT1、miRNA4459、LARP1、SQSTM1、CASP1、IL1B水平。结果与模型组相比,血管软化丸组TC、TG和LDL-C水平降低(均P<0.05),主动脉LA较大、IMT较薄、PA较小、LCA较小(P<0.05),主动脉TGFB2-OT1光密度值和荧光强度较低(均P<0.05),血清ICAM-1、VCAM-1、IL-8和MCP-1水平较低(均P<0.05),主动脉TGFB2-OT1、miRNA4459、LARP1、SQSTM1水平较低(均P<0.05),主动脉TGFB2-OT1、CASP1、IL1B蛋白表达水平较低(均P<0.05)。结论血管软化丸防治AS的分子机制与靶向调控长链非编码RNA-TGFB2-OT1、miR4459及其下游信号抑制炎症反应有关。 展开更多
关键词 动脉粥样硬化 长链非编码rna-tgfb2-ot1 血管软化丸 炎症反应
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