Inhibition of MARK2 inhibits ovarian cancer cell proliferation by regulating PI3K/AKT/p53 axis

IF 0.5 4区 医学 Q4 OBSTETRICS & GYNECOLOGY
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引用次数: 0

Abstract

Ovarian cancer (OC) is the 3rd most common type of the gynecological malignancy. Although current treatment strategies have greatly improved, there is still a need to develop new biomarkers for OC diagnosis and treatment. Microtubule affinity regulated kinase 2 (MARK2) is a kinase involved in the progression of multiple tumors. However, whether abnormal expression of MARK2 is associated with OC progression needs further analysis. We here revealed its role in OC. We found high expression of MARK2 in OC. Knockdown of MARK2 inhibited proliferation of OC cells, stimulated apoptosis of OC cells, and restrained glucose metabolism of OC cells. Furthermore, MARK2 regulated phosphatidylinositol 3-kinase/PKB (protein kinase B)/tumor suppressor protein 53 (PI3K/AKT/p53) axis in OC, therefore affecting the progression of OC. In summary, MARK2 knockdown suppressed cell proliferation by regulating PI3K/AKT/p53 axis.
抑制MARK2通过调控PI3K/AKT/p53轴抑制卵巢癌细胞增殖
卵巢癌(OC)是第三种最常见的妇科恶性肿瘤。虽然目前的治疗策略已经有了很大的改进,但仍需要开发新的生物标志物来诊断和治疗卵巢癌。微管亲和调节激酶2 (MARK2)是一种参与多发性肿瘤进展的激酶。然而,MARK2的异常表达是否与OC进展相关,还有待进一步分析。我们在这里揭示了它在OC中的作用。我们发现MARK2在OC中高表达。敲低MARK2抑制OC细胞增殖,刺激OC细胞凋亡,抑制OC细胞糖代谢。此外,MARK2调节OC中磷脂酰肌醇3-激酶/PKB(蛋白激酶B)/肿瘤抑制蛋白53 (PI3K/AKT/p53)轴,从而影响OC的进展。综上所述,MARK2敲低通过调控PI3K/AKT/p53轴抑制细胞增殖。
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来源期刊
自引率
25.00%
发文量
58
审稿时长
1 months
期刊介绍: EJGO is dedicated to publishing editorial articles in the Distinguished Expert Series and original research papers, case reports, letters to the Editor, book reviews, and newsletters. The Journal was founded in 1980 the second gynaecologic oncology hyperspecialization Journal in the world. Its aim is the diffusion of scientific, clinical and practical progress, and knowledge in female neoplastic diseases in an interdisciplinary approach among gynaecologists, oncologists, radiotherapists, surgeons, chemotherapists, pathologists, epidemiologists, and so on.
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