Sodium selenite inhibits the growth of cervical cancer cells through the PI3K/AKT pathway

Yuanyuan Wang; Lei Qi; Sihong Guo; Yuehui Jia; Ruixiang Wang; Cunqi Lv; Qingyu Zeng; Ying Gao; Tong Wang; Qi Li

doi:10.1016/j.jtemb.2024.127582

Sodium selenite inhibits the growth of cervical cancer cells through the PI3K/AKT pathway

J Trace Elem Med Biol. 2024 Dec 17:87:127582. doi: 10.1016/j.jtemb.2024.127582. Online ahead of print.

Authors

Yuanyuan Wang¹, Lei Qi², Sihong Guo³, Yuehui Jia¹, Ruixiang Wang¹, Cunqi Lv¹, Qingyu Zeng¹, Ying Gao⁴, Tong Wang⁵, Qi Li⁶

Affiliations

¹ Institute of Keshan Disease, Chinese Center for Endemic Disease Control, Harbin Medical University, Harbin 150081, China.
² Institute of Keshan Disease, Chinese Center for Endemic Disease Control, Harbin Medical University, Harbin 150081, China; School of Public Health, Qiqihar Medical University, Qiqihar, Heilongjiang 161006, China.
³ Department of Gynecological Oncology, The First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin 150006, China.
⁴ Department of Gynecological Oncology, Harbin Medical University Cancer Hospital, Harbin 150081, China. Electronic address: anna625@163.com.
⁵ Institute of Keshan Disease, Chinese Center for Endemic Disease Control, Harbin Medical University, Harbin 150081, China. Electronic address: wangtong@ems.hrbmu.edu.cn.
⁶ Department of Radiotherapy, Harbin Medical University Cancer Hospital, Harbin 150081, China. Electronic address: liqi@ems.hrbmu.edu.cn.

PMID: 39708662
DOI: 10.1016/j.jtemb.2024.127582

Abstract

Background: Selenium can inhibit cervical cancers, but the specific mechanism of anti-cervical cancer is not fully understood.

Methods: In this study, we investigated the anti-cervical cancer effect of sodium selenite (SS) in vivo and in vitro to reveal the role of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway in terms of the mechanism. In vivo experiments, HeLa cell xenografts were constructed in BALB/c female nude mice, and then intraperitoneally injected with 3 mg/kg sodium selenite (SS) for 14 days. In vitro experiments, we detected cell viability by MTT assay and apoptosis by Annexin V-FITC/PI staining. The levels of PI3K, AKT, phosphorylated PI3K (p-PI3K), and phosphorylated Akt (p-AKT) were measured by Western Blot.

Results: HeLa cell xenografts in female nude mice showed delayed tumor growth and no apparent toxicity in the liver or kidney. SS reduced the viability and increased apoptosis of HeLa and SiHa cells. SS did not affect PI3K and AKT levels and decreased p-PI3K and p-AKT levels. In addition, the results also revealed that the SS combined with LY294002, a specific PI3K inhibitor, enhanced the inhibitory effect of SS on the PI3K/AKT signaling pathway, further inhibiting cervical cancer cell viability and increased apoptosis.

Conclusions: SS exerted its anti-cervical cancer effects by inhibiting cell proliferation, promoting apoptosis, and inhibiting the PI3K/AKT signaling pathway.

Keywords: Apoptosis; Cervical cancer; PI3K/AKT signaling pathway; Sodium selenite; Viability.