ELOVL2 restrains cell proliferation, migration, and invasion of prostate cancer via regulation of the tumor suppressor INPP4B

前列腺癌 癌症研究 PI3K/AKT/mTOR通路 癌症 基因敲除 生物 前列腺 细胞生长 蛋白激酶B 病理 信号转导 医学 基因 遗传学
作者
Tengfei Hu,Hao Zhang,Yuguang Du,Shaoge Luo,Xinggang Yang,Hui Zhang,Jiarong Feng,Xiaohong Chen,Xuchong Tu,Chunlin Wang,Yan Zhang
出处
期刊:Cellular Signalling [Elsevier]
卷期号:96: 110373-110373 被引量:6
标识
DOI:10.1016/j.cellsig.2022.110373
摘要

Prostate cancer is one of the most common malignancies in men. Members of the elongation of the very-long-chain fatty acid (ELOVL) gene family have been reported to participate in the occurrence and development of various cancers. However, the function of ELOVL gene family members (ELOVLs) in prostate cancer has not been fully elucidated. The mRNA expression and prognostic value of ELOVLs in prostate cancer were analyzed using the GEPIA database. The Oncomine database and PrognoScan database were used to further verify the mRNA expression level and prognostic value of ELOVL2 in prostate cancer. RT–qPCR and Western blotting were used to validate the expression levels of ELOVL2 in four prostate cancer cell lines. Immunohistochemistry was performed to detect the ELOVL2 protein expression levels in prostate cancer tissues. Coexpression analysis in the cBioPortal database and enrichment analysis in Kyoto Encyclopedia of Genes and Genomes (KEGG), CCK8, colony formation, and transwell assays were used to identify the functions and mechanisms of ELOVL2. ELOVL2 expression was upregulated in prostate cancer tissues compared with normal tissues. High expression of ELOVL2 indicated a better prognosis in prostate cancer patients. ELOVL2 expression was negatively correlated with Gleason score. Knockdown of ELOVL2 promoted cell proliferation, colony formation, migration, invasion, and the growth of subcutaneous xenografts and activated the PI3K/Akt signaling pathway by downregulating INPP4B, while overexpression of ELOVL2 reversed these effects. In addition, overexpression of INPP4B blocked the promoting effect of sh-ELOVL2 on cell proliferation, colony formation, migration, invasion, and the PI3K/Akt signaling pathway. Our findings suggest that ELOVL2 might be a prognostic biomarker and therapeutic target for prostate cancer.
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
更新
大幅提高文件上传限制,最高150M (2024-4-1)

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
斯文败类应助孔雀翎采纳,获得10
1秒前
想发文章的小菜鸟完成签到,获得积分10
1秒前
Zymiao完成签到,获得积分20
1秒前
小易完成签到,获得积分10
1秒前
qu完成签到 ,获得积分20
1秒前
谷贝贝发布了新的文献求助10
2秒前
温暖完成签到,获得积分20
2秒前
susiex发布了新的文献求助10
2秒前
2秒前
去看海嘛应助phantom采纳,获得10
3秒前
cuin0发布了新的文献求助10
3秒前
3秒前
之桃完成签到,获得积分10
3秒前
4秒前
4秒前
4秒前
5秒前
wnll完成签到,获得积分10
5秒前
6秒前
Ava应助顺心的飞丹采纳,获得10
6秒前
充电宝应助大眼的平松采纳,获得10
6秒前
7秒前
7秒前
ykd发布了新的文献求助10
7秒前
去看海嘛应助phantom采纳,获得10
7秒前
李龙波完成签到,获得积分10
7秒前
哈喽酷狗发布了新的文献求助10
7秒前
海莲发布了新的文献求助10
8秒前
勤恳冬萱发布了新的文献求助10
9秒前
Ll完成签到,获得积分20
9秒前
9秒前
9秒前
明亮的智宸完成签到,获得积分10
9秒前
大模型应助萧水白采纳,获得100
9秒前
cuin0完成签到,获得积分10
9秒前
wnll发布了新的文献求助10
9秒前
胡强完成签到,获得积分10
10秒前
华仔应助张张采纳,获得30
10秒前
笨笨石头完成签到,获得积分10
10秒前
我是老大应助欣慰小丸子采纳,获得10
11秒前
高分求助中
Evolution 10000
The Young builders of New china : the visit of the delegation of the WFDY to the Chinese People's Republic 1000
юрские динозавры восточного забайкалья 800
English Wealden Fossils 700
Foreign Policy of the French Second Empire: A Bibliography 500
Chen Hansheng: China’s Last Romantic Revolutionary 500
China's Relations With Japan 1945-83: The Role of Liao Chengzhi 400
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3147582
求助须知:如何正确求助?哪些是违规求助? 2798713
关于积分的说明 7830993
捐赠科研通 2455488
什么是DOI,文献DOI怎么找? 1306841
科研通“疑难数据库(出版商)”最低求助积分说明 627934
版权声明 601587