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Sodium selenite inhibits cervical cancer progression via ROS-mediated suppression of glucose metabolic reprogramming
Qingyu Zeng1, Cunqi Lv1, Lei Qi2
1Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, Heilongjiang Province, China; Key Lab of Etiology and Epidemiology, Education Bureau of Heilongjiang Province, Ministry of Health (23618504), Harbin Medical University, Harbin 150081, Heilongjiang Province, China.
Aims:
This study aims to explore the inhibitory effect of selenium on cervical cancer through suppression of glucose metabolic reprogramming and its underlying mechanisms.
Methods:
Sodium selenite (SS) treated HeLa and SiHa cells were assessed for proliferation using the CCK-8 assay and immunofluorescence. DNA synthesis was measured with the EdU assay. A nude mouse xenograft model evaluated SS's anti-cervical cancer effects. Reactive oxygen species (ROS) and mitochondrial membrane potential were measured using flow cytometry, DCFH-DA, and JC-1 probes, respectively. Apoptosis was detected via Annexin V/PI staining and Western blot. Glucose uptake, lactate production, and ATP generation were determined using 2-NBDG probes and assay kits. The mRNA and protein levels of glycolysis-related genes HK2, GLUT1, and PDK1 were measured using RT-qPCR and Western blot.
Key Findings:
SS inhibited HeLa and SiHa cells viability in a dose- and time-dependent manner. Intraperitoneal injection of SS in nude mice significantly inhibited HeLa cell xenograft growth without evident hepatotoxicity or nephrotoxicity. SS inhibited glucose metabolic reprogramming in cancer cells primarily via ROS-mediated AKT/mTOR/HIF-1α pathway inhibition. Pretreatment with N-acetylcysteine (NAC) or MHY1485 (an mTOR activator) partially reversed the inhibitory effects of SS on glucose metabolic reprogramming, cell proliferation, and migration, as well as its pro-apoptotic effects.
Significance:
SS exhibited anti-cervical cancer effects, likely through the induction of ROS generation and inhibition of glucose metabolic reprogramming in cervical cancer cells, thereby inhibiting cell proliferation and promoting apoptosis. These findings provide new insights into understanding the molecular mechanisms underlying SS for potential new drug development for cervical cancer.
Insights
Selenium supplementation inhibits cervical cancer by disrupting cancer cell metabolism. This research reveals how selenium targets glucose reprogramming, offering potential for new cervical cancer treatments.
Area of Science:
- Oncology
- Biochemistry
- Molecular Biology
Background:
- Cervical cancer exhibits altered glucose metabolism for rapid proliferation.
- Targeting metabolic pathways presents a therapeutic strategy for cervical cancer.
- Selenium's role in cancer prevention and treatment is under investigation.
Purpose of the Study:
- To investigate the inhibitory effects of selenium on cervical cancer.
- To explore selenium's impact on glucose metabolic reprogramming in cervical cancer cells.
- To elucidate the underlying molecular mechanisms, including reactive oxygen species (ROS) generation and apoptosis induction.
Main Methods:
- Cell viability, DNA synthesis, and apoptosis were assessed in HeLa and SiHa cells treated with sodium selenite (SS).
- A nude mouse xenograft model was used to evaluate SS's in vivo anti-cancer effects.
- Glucose uptake, lactate production, ATP generation, and key glycolysis-related gene expression (HK2, GLUT1, PDK1) were measured.
- ROS levels and mitochondrial membrane potential were analyzed using flow cytometry.
Main Results:
- Sodium selenite (SS) significantly inhibited cervical cancer cell viability and xenograft growth in mice.
- SS suppressed glucose metabolic reprogramming by inhibiting the ROS-mediated AKT/mTOR/HIF-1α pathway.
- SS treatment induced apoptosis and inhibited cell proliferation and migration.
- N-acetylcysteine (NAC) or an mTOR activator partially reversed SS's inhibitory effects.
Conclusions:
- Selenium exhibits anti-cervical cancer properties by inducing ROS and inhibiting glucose metabolic reprogramming.
- These mechanisms lead to decreased cell proliferation and increased apoptosis in cervical cancer cells.
- The findings support selenium's potential as a therapeutic agent for cervical cancer, warranting further drug development.
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