<scp>PDCD10</scp> promotes proliferation, migration, and invasion of osteosarcoma by inhibiting apoptosis and activating <scp>EMT</scp> pathway

骨肉瘤 细胞凋亡 细胞生长 癌症研究 生物 医学 遗传学
作者
Ke Xu,Wenchao Fei,Ziqi Huo,Shuoer Wang,Yinghua Li,Gong Yang,Yang Hong
出处
期刊:Cancer Medicine [Wiley]
标识
DOI:10.1002/cam4.5025
摘要

Osteosarcoma, a common primary malignant tumor, occurs in children and adolescents with a poor prognosis. The current treatment methods are various, while the five-year survival rate of patients has not been significantly improved. As a member of the programmed death factor (PDCD) family, programmed death factor 10 (PDCD10) plays a role in regulating cell apoptosis. Several studies of PDCD10 in CCM and cancers have been reported before. However, there are no relevant research reports on the effects of PDCD10 on osteosarcoma.We used bioinformatics analysis, IHC, and clinical data to confirm the expression of PDCD10 and its correlation with prognosis in osteosarcoma. Then, we used shRNAs and cDNA to knock down or overexpress PDCD10 in U2OS and MG63 cell lines. A series of function assays such as CCK8, Wound healing test, Plate cloning formation assay, and Transwell were done to confirm how PDCD10 affects osteosarcoma. Animal assays were done to confirm the conclusions in cell lines. At last, WB was used to measure the protein expression levels of apoptosis and the EMT pathway.PDCD10 was highly expressed in patients with osteosarcoma and correlated with prognosis; PDCD10 knockdown inhibited osteosarcoma growth, proliferation, migration, and invasion; PDCD10 overexpression promoted osteosarcoma growth, proliferation, migration, and invasion. In vivo experiments confirmed the conclusions in cell lines; PDCD10 inhibited apoptosis and activated the EMT pathway.In this study, it was found that PDCD10 was highly expressed in patients with osteosarcoma, and it was closely related to patient prognosis. PDCD10 inhibited tumor cell apoptosis and promoted tumor progression by activating the EMT pathway. These findings may provide a potential target for gene therapy of osteosarcoma.
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
normalgai完成签到,获得积分10
2秒前
务实幼蓉发布了新的文献求助10
2秒前
zhaoyingxin发布了新的文献求助10
3秒前
慕容飞凤发布了新的文献求助30
4秒前
MQ&FF发布了新的文献求助10
4秒前
5秒前
yy完成签到,获得积分20
5秒前
叶子完成签到,获得积分10
5秒前
周一发布了新的文献求助10
5秒前
helinahs完成签到 ,获得积分10
7秒前
7秒前
天天快乐应助HYT采纳,获得10
7秒前
晓先森完成签到,获得积分10
8秒前
9秒前
bong发布了新的文献求助10
9秒前
15966014069发布了新的文献求助10
11秒前
调研昵称发布了新的文献求助10
11秒前
周一完成签到,获得积分10
11秒前
11秒前
科目三应助小九不太乖采纳,获得10
12秒前
normalgai关注了科研通微信公众号
13秒前
bong完成签到,获得积分10
17秒前
星辰大海应助kk采纳,获得10
18秒前
19秒前
19秒前
Jasper应助帆帆帆采纳,获得10
20秒前
MQ&FF完成签到,获得积分0
20秒前
20秒前
坚定的雁完成签到 ,获得积分10
20秒前
20秒前
20秒前
大个应助科研通管家采纳,获得10
23秒前
科研通AI2S应助科研通管家采纳,获得10
23秒前
SciGPT应助科研通管家采纳,获得10
23秒前
完美世界应助科研通管家采纳,获得10
23秒前
共享精神应助qqqqgc采纳,获得10
23秒前
bkagyin应助科研通管家采纳,获得10
23秒前
852应助科研通管家采纳,获得10
23秒前
科研通AI2S应助科研通管家采纳,获得10
23秒前
情怀应助科研通管家采纳,获得10
23秒前
高分求助中
Evolution 10000
юрские динозавры восточного забайкалья 800
English Wealden Fossils 700
Mantiden: Faszinierende Lauerjäger Faszinierende Lauerjäger 600
Distribution Dependent Stochastic Differential Equations 500
A new species of Coccus (Homoptera: Coccoidea) from Malawi 500
A new species of Velataspis (Hemiptera Coccoidea Diaspididae) from tea in Assam 500
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 3157329
求助须知:如何正确求助?哪些是违规求助? 2808824
关于积分的说明 7878475
捐赠科研通 2467158
什么是DOI,文献DOI怎么找? 1313222
科研通“疑难数据库(出版商)”最低求助积分说明 630369
版权声明 601919