已入深夜,您辛苦了!由于当前在线用户较少,发布求助请尽量完整地填写文献信息,科研通机器人24小时在线,伴您度过漫漫科研夜!祝你早点完成任务,早点休息,好梦!

Exosome-transmitted hsa_circ_0012634 suppresses pancreatic ductal adenocarcinoma progression through regulating miR-147b/HIPK2 axis

作者
Luoluo Wang,Xiang Wu,Yi Ruan,Xueming Zhang,Xinhua Zhou
出处
期刊:Cancer Biology & Therapy [Taylor & Francis]
卷期号:24 (1): 2218514-2218514 被引量:16
标识
DOI:10.1080/15384047.2023.2218514
摘要

Circular RNA (circRNA) has been confirmed to play a vital role in pancreatic ductal adenocarcinoma (PDAC) progression. However, the function and regulatory mechanism of hsa_circ_0012634 in PDAC progression remain unclear. Quantitative real-time PCR was used to measure the expression of hsa_circ_0012634, microRNA (miR)-147b and homeodomain interacting protein kinase 2 (HIPK2). Cell function was assessed by cell counting kit 8 assay, EdU assay, colony formation assay and flow cytometry. Glucose uptake and lactate production were evaluated to determine cell glycolysis ability. Protein expression was examined by western blot analysis. RNA interaction was confirmed by RNA pull-down assay and dual-luciferase reporter assay. Exosomes were isolated from serums and cell culture supernatant using ultracentrifugation and identified by transmission electron microscopy. Animal experiments were conducted using nude mice. Hsa_circ_0012634 was downregulated in PDAC tissues and cells, and its overexpression suppressed PDAC cell proliferation, glycolysis and enhanced apoptosis. MiR-147b was targeted by hsa_circ_0012634, and its inhibitors repressed PDAC cell growth and glycolysis. HIPK2 could be targeted by miR-147b, and hsa_circ_0012634 regulated miR-147b/HIPK2 to suppress PDAC cell progression. Hsa_circ_0012634 was lowly expressed in serum exosomes of PDAC patients. Exosomal hsa_circ_0012634 inhibited PDAC cell growth and glycolysis in vitro, as well as tumorigenesis in vivo. Exosomal hsa_circ_0012634 restrained PDAC progression via the miR-147b/HIPK2 pathway, confirming that hsa_circ_0012634 might serve as a diagnosis and treatment biomarker for PDAC.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
和谐的山水完成签到,获得积分10
2秒前
深情安青的应助被优美妙柏采纳,获得20
2秒前
星辰大海完成签到 ,获得积分10
3秒前
ccc完成签到 ,获得积分10
3秒前
酒窝小羊完成签到,获得积分20
4秒前
翔空完成签到,获得积分10
5秒前
冷静的兰完成签到,获得积分10
5秒前
隐形曼青的应助被酸味yjm采纳,获得10
6秒前
孝顺的怜寒完成签到,获得积分10
9秒前
CodeCraft的应助被lizhengguang采纳,获得10
12秒前
xyyyy完成签到 ,获得积分10
13秒前
李健的粉丝团团长的应助被dq采纳,获得10
13秒前
16秒前
王jr完成签到 ,获得积分10
19秒前
LiyanShen完成签到,获得积分10
20秒前
锅包又完成签到 ,获得积分10
21秒前
tabblk完成签到 ,获得积分10
21秒前
alan完成签到 ,获得积分0
22秒前
酸味yjm发布了新的文献求助10
22秒前
23秒前
26秒前
YiYang完成签到 ,获得积分10
26秒前
More的应助被LiyanShen采纳,获得10
26秒前
乔舟完成签到 ,获得积分10
26秒前
27秒前
29秒前
30秒前
Helen完成签到 ,获得积分10
31秒前
杜康完成签到,获得积分10
31秒前
优美妙柏发布了新的文献求助20
32秒前
32秒前
睡个好觉啦完成签到 ,获得积分10
32秒前
赵赶超完成签到,获得积分10
33秒前
小魏发布了新的文献求助10
33秒前
灵巧幻露完成签到,获得积分10
33秒前
34秒前
lizhengguang发布了新的文献求助10
35秒前
橘生淮北1021完成签到 ,获得积分10
36秒前
彭晶晶完成签到 ,获得积分10
36秒前
6666发布了新的文献求助200
36秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Energie-Contracting 1500
Klimaschutzrecht durch den Energiesektor im Mehrebenensystem – Ein Rechtsvergleich 1000
Oncology Clinical Trials: Successful Design, Conduct, and Analysis, Second Edition 800
Exploring Mental Health in Education 600
Stochastic Models in Operations Research,Vol. 2 600
Organizational Behavior 510
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 计算机科学 工程类 有机化学 化学工程 生物化学 物理 复合材料 内科学 催化作用 光电子学 人工智能 细胞生物学 无机化学 物理化学 数学
热门帖子
关注 科研通微信公众号,转发送积分 8049190
求助须知:如何正确求助?哪些是违规求助? 9478502
关于积分的说明 21293229
捐赠科研通 7617509
什么是DOI,文献DOI怎么找? 3392905
关于科研通互助平台的介绍 2524126
邀请新用户注册赠送积分活动 2430940