- 4
- 0
- 约11.96万字
- 约 101页
- 2021-04-15 发布于江苏
- 举报
第三军医大学博士学位论文Reaction
第三军医大学博士学位论文
Reaction
Tris Tris(hydroxylmethyl)aminomethane 三羟甲基氨基甲烷 CCK8 Cell Counting Kit一8 细胞计数试剂盒 Real time PCR Real time Polymerase Chain Reaction 实时定量PCR 0D Optical Density 光密度
TBST Tris Buffered Saline with Tween 20 TBST缓冲液
rpm Revolutions per minute 姨|食
CY3 Cyanine 3 青蓝3荧光素
EB ethidium bromide 溴化乙锭
EP—CAM epithelial cell adhesion molecule 上皮细胞粘附分子 PAGE Polyacrylamide Gel Electrophoresis 聚丙烯酰胺凝胶电泳 TICs Tumour initiating cells 肿瘤始动细胞
PTPN4 protein tyrosine phosphatase non-receptor 蛋白酪氨酸磷酸化非受体4
type4
SP Side Population Cells 侧群细胞
PCR Polymerase Chain Reaction 聚合酶链反应
RAB member RAS oncogene family RAS癌基因家族
PDCD4 programmed cell death 4 程序性细胞死亡蛋白4
TEMED tetramethylethylenediamine 四甲基乙二胺
2
万方数据
第三军医大学博士学位论文MicroRNA-183
第三军医大学博士学位论文
MicroRNA-183 promotes motility of CDl33+/CD326+ CSLCs through PTPN4 repression
Abstract
Background
Non·small cell lung cancer(NSCLC)is one of the most common cancers worldwide and ranks a leading cause of lung cancer mortality partly due to distant metastasis even in the early stages.An increasing number of studies have revealed that primary tumors contain a rare subpopulation of cells,termed cancer stem-like cells(CSLCs)or tumor initiating cells(TICs) that possess stronger invasiveness to form metastases in remote organs.
MicroRNAs(miRNAs)are class of small,endogenous,non—coding RNAs that negatively regulate gene expression by partial or entire complementary binding to 3untranslatedregion(UT鼬of mRNAs.Emerging evidence reveals that abnormal miRNA expression is relevant to the dysregulation of CSLCs in various cancers such as miR一1 8 1 and hepatic CSLCs,miR34 and pancreatic CSLCs,miR-340 and glioma CSLCs,miR一125a and
breast CSLCs,miR-17 and ovarian CSLCs,miR-146a and colorectal CSLCs,and miR-320
and prostate CSLCs.
Previous studies revealed that miR一1 83 Can mediate the invasiveness and growth of NSCLC.However,the exact role ofmiR·183 in regulating the biological behavior ofCSLCs in NSCLC remains unclear.Thus,a bet
原创力文档

文档评论(0)