Expression of p-Akt in ovarian serous carcinoma and its association with proliferation and apoptosis

Abstract

The aim of the present study was to determine the expression of p-Akt in ovarian serous carcinoma (OSC) and its association with proliferation and apoptosis. Paraffin-embedded tissues of patients aged between 35 and 64 years old without history of radiotherapy, chemotherapy and hormone therapy prior to surgery were collected. In total, samples included 12 ovarian serous cystadenomas (OSAs), 18 ovarian serous borderline tumors (OS-BTs) and 46 OSCs. Of the 46 OSC samples, 16 were well-differentiated, 20 were moderately differentiated and 10 were poorly differentiated, while 22 developed lymphatic metastases and 24 were metastasis-free. An additional 10 paraffin-embedded normal ovarian tissues (NOTs) were used as controls. Streptavidin-peroxidase immunohistochemistry assays were used to investigate the expression of p-Akt and cyclin D1 in the collected samples. Compared with NOT, p-Akt expression in the OS-BT and OSC groups, as well as cyclin D1 expression in the OSA and OSC groups, was significantly elevated (P<0.05). Compared with the OSA group, p-Akt expression in the OSC group was significantly elevated (P<0.01) and reversely associated with tumor differentiation (P<0.01), whereas cyclin D1 expression showed no correlation with tumor differentiation (P>0.05). The expression of p-Akt, caspase-3 and cyclin D1 was positively associated with lymphatic metastasis (r=0.334; P=0.023). The expression of p-Akt gradually increased with carcinoma development and was associated with differentiation and metastasis of OSC, revealing that the activation of the PI3K/Akt signaling pathway is involved in the development of OSC. Furthermore, the expression of cyclin D1 gradually increased in the NOT, OSA, OS-BT and OSC groups and was associated with tumor metastasis.

Low-Frequency Magnetic Fields (LF-MFs) Inhibit Proliferation by Triggering Apoptosis and Altering Cell Cycle Distribution in Breast Cancer Cells

“…The PI3K/AKT/ GSK3β signaling pathway is one of the important signal transduction pathways, playing an anti-apoptosis and survival-promoting role in cells by activating a variety of downstream effector molecules [30]. Some studies showed that the signaling pathway is closely related to the occurrence and development of a variety of common malignant tumors, as the expressions of p-AKT and p-GSK3β are significantly higher than those in normal tissues within tumors like glioma, ovarian carcinoma, and breast carcinoma [31][32][33][34]. Hongen Lei et al showed that LF-MF decreased human prostatic adenocarcinoma cell proliferation and the activity of AKT pathway [35].…”

Telmisartan inhibits NSCLC A549 cell proliferation and migration by regulating the PI3K/AKT signaling pathway

“…AKT has direct effects on the effectors of the apoptotic pathway, including Bcl-2 (38). Bcl-2 activity is regulated via p-AKT in various cell types (39). AKT phosphorylates Bax, disrupting its interaction with Bcl-XL to protect cells from apoptosis (40).…”