HAGLROS promotes cell proliferation and angiogenesis and inhibits apoptosis by activating multiple signaling pathways in LSCC cells

血管生成 蛋白激酶B 增殖细胞核抗原 细胞生物学 细胞凋亡 癌症研究 细胞生长 激酶 分子生物学 信号转导 流式细胞术 生物 磷酸化 生物化学
作者
Yunxia Ma,Hui Zhang,Xiaohong Li,Yehai Liu
出处
期刊:Journal of Oral Pathology & Medicine [Wiley]
卷期号:51 (6): 510-519 被引量:6
标识
DOI:10.1111/jop.13249
摘要

HAGLROS is a long noncoding RNA involving in the development of a variety of cancers, but its mechanism of action in laryngeal squamous cell carcinomas (LSCC) is still unclear. We aim to unveil the effect and mechanism of HAGLROS on LSCC.The expression of HAGLROS in LSCC patients' tissues, serum, and LSCC cell lines was quantified by quantitative real-time PCR. AMC-HN-8 and SNU-46 cells were transfected with the overexpression plasmid of HAGLROS and shHAGLROS, and the functional assay (colony formation assays, flow cytometry, and tube formation) was performed. Western blot was used to determine the expressions of vascular endothelial growth factor (VEGF), proliferating cell nuclear antigen (PCNA), P27 and cleaved caspase-3, as well as phosphorylated-c-Jun-N-terminal kinase (p-JNK), JNK, phosphorylated-extracellular signal-regulated kinase 1/2 (p-Erk1/2), Erk1/2, phosphorylated-protein kinase B (p-AKT) and AKT.HAGLROS was highly expressed in LSCC tissues and cells, and it was correlated to lymph node, tumor depth, and clinical stage of LSCC patients. The proliferation ability of LSCC cells was higher than that of HuLa-PC cells. Meanwhile, HAGLROS overexpression promoted the abilities of proliferation and angiogenesis and reduced apoptosis, whereas silencing of HAGLROS exerted the opposite effects in LSCC cell lines. Moreover, overexpressed HAGLROS upregulated the expressions of VEGF and PCNA yet downregulated the expressions of P27 and cleaved caspase-3 by activating Erk1/2 and AKT or JNK signaling pathways in different LSCC cell lines.Overexpressed HAGLROS promoted the proliferation and angiogenesis yet inhibited apoptosis of LSCC cells by activating Erk1/2 and AKT or JNK signaling pathways.
最长约 10秒,即可获得该文献文件

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
lolly发布了新的文献求助20
刚刚
刚刚
12356完成签到,获得积分10
刚刚
刚刚
呆萌的奄完成签到,获得积分10
1秒前
运敬完成签到 ,获得积分10
1秒前
万能图书馆应助科研dog采纳,获得10
1秒前
Bown发布了新的文献求助30
1秒前
chongchong发布了新的文献求助10
4秒前
科研通AI2S应助科研通管家采纳,获得10
4秒前
粒子发布了新的文献求助80
4秒前
haix应助科研通管家采纳,获得10
4秒前
星辰大海应助科研通管家采纳,获得10
4秒前
休亮完成签到,获得积分10
4秒前
我是老大应助科研通管家采纳,获得10
5秒前
香蕉觅云应助科研通管家采纳,获得10
5秒前
Jasper应助科研通管家采纳,获得10
5秒前
彭于晏应助科研通管家采纳,获得10
5秒前
大模型应助科研通管家采纳,获得10
5秒前
充电宝应助科研通管家采纳,获得30
5秒前
所所应助科研通管家采纳,获得10
5秒前
JamesPei应助科研通管家采纳,获得10
5秒前
情怀应助科研通管家采纳,获得10
5秒前
赘婿应助科研通管家采纳,获得10
5秒前
haix应助科研通管家采纳,获得10
5秒前
华仔应助科研通管家采纳,获得10
5秒前
在水一方应助科研通管家采纳,获得10
5秒前
丘比特应助科研通管家采纳,获得10
5秒前
传奇3应助科研通管家采纳,获得10
5秒前
祝你勇敢应助科研通管家采纳,获得10
5秒前
lightman完成签到,获得积分10
6秒前
7秒前
xu发布了新的文献求助10
7秒前
善良的剑通应助子云采纳,获得20
8秒前
9秒前
rachel03发布了新的文献求助10
10秒前
11秒前
11秒前
12秒前
谢晓东完成签到,获得积分10
12秒前
高分求助中
Applied Survey Data Analysis (第三版, 2025) 800
Assessing and Diagnosing Young Children with Neurodevelopmental Disorders (2nd Edition) 700
Images that translate 500
Algorithmic Mathematics in Machine Learning 500
Handbook of Innovations in Political Psychology 400
Mapping the Stars: Celebrity, Metonymy, and the Networked Politics of Identity 400
Nucleophilic substitution in azasydnone-modified dinitroanisoles 300
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3842525
求助须知:如何正确求助?哪些是违规求助? 3384644
关于积分的说明 10536237
捐赠科研通 3105132
什么是DOI,文献DOI怎么找? 1710053
邀请新用户注册赠送积分活动 823486
科研通“疑难数据库(出版商)”最低求助积分说明 774091