Редактирование: ADRA2A

Alpha-2A adrenergic receptor (Alpha-2 adrenergic receptor subtype C10) (Alpha-2A adrenoreceptor) (Alpha-2A adrenoceptor) (Alpha-2AAR) [ADRA2R] [ADRAR]

==Publications==

{{medline-entry
|title=α2A-Adrenergic Receptor Inhibits the Progression of Cervical Cancer Through Blocking PI3K/AKT/mTOR Pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33116632
|abstract=The study aimed to investigate the effect of α2A-adrenergic receptor ([[ADRA2A]]) on cervical cancer and the potential mechanisms of [[ADRA2A]] on phosphatidylinositol 3'-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway in cervical cancer cells. In our study, [[ADRA2A]] expression was evaluated by analyzing cervical cancer RNA sequencing dataset from the GEPIA. The prognostic values of [[ADRA2A]] were evaluated by Kaplan-Meier method using the Cancer Genome Atlas (TCGA) database data. In addition, the expression of [[ADRA2A]] in cervical cancer cell lines was detected by qRT-PCR and Western blot. Subsequently, the roles of [[ADRA2A]] on cell proliferation, apoptosis, migration, invasion and senescence in HeLa and SiHa cells were evaluated. Moreover, tumorigenesis in nude mice was used to investigate the role of [[ADRA2A]] in vivo. We also detected the expression changes of key factors in PI3K/Akt/mTOR pathway after overexpression and silencing of [[ADRA2A]] in HeLa and SiHa cells. [[ADRA2A]] expression was significantly downregulated in cervical cancer tissues and cell lines. The high expression of [[ADRA2A]] was significantly associated with a better prognosis in cervical cancer patients. [[ADRA2A]] overexpression significantly suppressed cell proliferation, migration and invasion, and promoted cell senescence and apoptosis in cervical cancer cells. On the contrary, silencing [[ADRA2A]] dramatically facilitated cell proliferation, migration and invasion, and inhibited cell senescence and apoptosis in cervical cancer cells. The expressions of p-PI3K, p-AKT and p-mTOR in cervical cancer cells were notably decreased by [[ADRA2A]] overexpression and increased by silencing [[ADRA2A]]. In addition, we also confirmed that [[ADRA2A]] overexpression could suppress the xenograft tumor growth in vivo. Our study demonstrated that [[ADRA2A]] could suppress cell proliferation, migration and invasion, as well as promote cell senescence and apoptosis through inhibiting PI3K/Akt/mTOR pathway in cervical cancer.

|keywords=* ADRA2A
* PI3K/Akt/mTOR pathway
* cervical cancer
* metastasis
* proliferation
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574911
}}