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Updated: Jun 16, 2025
Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
MiR-93-5p inhibits ovarian cancer through SLC7A11-mediated-ferroptosis
Chunxia Li1, Zitao Wang2, Yanqing Wang2
1Department of Obstetrics and Gynecology, Wuhan Wuchang Hospital, Wuhan, Hubei, 430065, China.
Aim:
Ovarian cancer (OC) is the most lethal gynecological malignancy, which seriously affects the prognosis and life quality of female patients. Therefore, new therapeutic targets and treatments are urgently needed.
Methods:
Expression levels of miR-93-5p and SLC7A11 and ferroptosis status in paracancerous and tumor tissues were examined and compared. The effect of the miR-93-5p-SLC7A11 regulatory loop on the malignant phenotype as well as the ferroptosis phenotype of SKOV3 cells was assessed. Furthermore, the interaction between miR-93-5p and SLC7A11 was confirmed via rescue experiment.
Results:
In this study, we found that miR-93-5p was lowly expressed in cancer tissues, and suggested that overexpression of miR-93-5p could target SLC7A11 to reduce its expression and promote ferroptosis, thereby inhibiting the malignant biological behaviors such as proliferation, invasion and migration, while knockdown of miR-93-5p restrained ferroptosis and promoting tumor growth. Besides, erastin, as a specific inhibitor of SLC7A11, could target down the expression of SLC7A11, induce the occurrence of ferroptosis, and reverse the effect of knockdown of miR-93-5p.
Conclusions:
Taken together, our findings disclosed that miR-93-5p increased the level of ferroptosis and inhibited the progression of OC by targeting and inhibiting the expression level of SLC7A11, which was a potential treatment in OC.
Insights
MicroRNA-93-5p (miR-93-5p) inhibits ovarian cancer (OC) progression by promoting ferroptosis. Overexpression of miR-93-5p targets SLC7A11, reducing its expression and hindering tumor growth.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Ovarian cancer (OC) is a leading cause of cancer-related death in women, necessitating novel therapeutic strategies.
- Identifying new molecular targets is crucial for improving OC patient prognosis and quality of life.
Purpose of the Study:
- To investigate the role of miR-93-5p and SLC7A11 in OC progression.
- To elucidate the regulatory relationship between miR-93-5p and SLC7A11 in the context of ferroptosis.
- To assess the therapeutic potential of targeting the miR-93-5p-SLC7A11 axis in OC.
Main Methods:
- Comparative analysis of miR-93-5p and SLC7A11 expression in OC tissues and adjacent normal tissues.
- In vitro studies using SKOV3 cells to assess the impact of miR-93-5p modulation on malignant and ferroptosis phenotypes.
- Rescue experiments to confirm the interaction between miR-93-5p and SLC7A11.
Main Results:
- miR-93-5p was found to be downregulated in OC tissues.
- Overexpression of miR-93-5p suppressed OC cell proliferation, invasion, and migration by targeting SLC7A11 and promoting ferroptosis.
- Knockdown of miR-93-5p enhanced ferroptosis resistance and promoted tumor growth, effects reversed by SLC7A11 inhibition with erastin.
Conclusions:
- miR-93-5p acts as a tumor suppressor in OC by enhancing ferroptosis via SLC7A11 downregulation.
- The miR-93-5p-SLC7A11 pathway represents a promising therapeutic target for ovarian cancer treatment.
