Molecular medicine reports · 2017
AKAP2 is upregulated in ovarian cancer, and promotes growth and migration of cancer cells.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Li Xin, Wang Changjun, Zhang Gang, Liang Ming, Zhang Bin
Аннотация
Mutations of A‑kinase anchoring protein 2 (AKAP2) have been reported to be associated with adolescent idiopathic scoliosis. However, its role in cancer is poorly understood. In the present study, the mRNA levels of AKAP2 in ovarian cancer tissues were examined using qPCR. The effects of AKAP2 on the growth and migration of cancer cells were examined using crystal violet and Boyden chamber assays. An in vivo image system was used to evaluate the effect of AKAP2 on the metastasis of ovarian cancer cells. The present study demonstrated that the expression of AKAP2 was elevated in ovarian cancer. Furthermore, overexpression of AKAP2 promoted the growth and migration of ovarian cancer cells, whereas knockdown of AKAP2 expression reduced the growth and migration of ovarian cancer cells. Analysis of the molecular mechanism indicated that AKAP2 activated β‑catenin/T cell factor signaling and regulated the expression of several target genes. Furthermore, analysis of the in vivo metastatic capacity demonstrated that downregulation of AKAP2 inhibited the invasion of ovarian cancer cells. Taken together, the present study demonstrated an oncogenic role for AKAP2 in ovarian cancer, indicating that AKAP2 may be a therapeutic target for ovarian cancer.
Предметные рубрики MeSH
A Kinase Anchor ProteinsAgedAnimalsCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesGenes, ReporterHeterograftsHumansMembrane ProteinsMiceMiddle AgedMutationNeoplasm StagingOvarian NeoplasmsRNA InterferenceSignal TransductionTCF Transcription Factorsbeta Catenin