Related Experiment Video
Updated: May 26, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
RNF112 mediates immunosuppression to inhibit the proliferation of cervical cancer by Foxm1
Huiying Pan1, Lei Bao2, Wei Shi1
1Department of Gynecological Oncology, The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Key Laboratory of Embryo Original Diseases, Shanghai, China.
Background:
Cervical cancer ranks as the fourth most common malignant tumor among women worldwide. However, the molecular mechanisms driving tumor progression and immune evasion in this disease have not been sufficiently clarified. The aim of this study was to determine the expression profile and clinical significance of ring finger protein 112 (RNF112) in cervical cancer and to elucidate the molecular mechanism by which RNF112 regulates tumor proliferation and immune response.
Methods:
The expression of RNF112 in tumor tissues from patients with cervical cancer and from healthy controls was analyzed via quantitative polymerase chain reaction and Western blotting. The correlation between RNF112 expression and survival of patients with cervical cancer was analyzed. The human immortalized cervical epithelial cell line (H8) and cervical cancer cell lines were used for in vitro experiments. To assess tumor growth in vivo, a xenograft mouse model of cervical cancer with RNF112 knockdown (shRNF112) was established. A co-culture system was employed to evaluate the interaction between cervical cancer cells and T lymphocytes. Oxidative stress levels, mitochondrial dysfunction, ferroptosis markers in T lymphocytes, and the ubiquitination level of Foxm1 were further detected.
Results:
RNF112 expression was significantly downregulated in both cervical cancer patient tissues and cell lines as compared to that from samples of healthy controls. Clinical analysis revealed that low RNF112 expression was associated with poor prognosis. In the mouse model, sh-RNF112 significantly promoted tumor growth. In terms of mechanism, RNF112 was found to alleviate the immunosuppressive state within the tumor microenvironment (TME). Specifically, RNF112 reduced oxidative stress, mitigated mitochondrial dysfunction, and suppressed ferroptosis in T lymphocytes. Furthermore, RNF112 promoted the ubiquitination and degradation of Foxm1; conversely, inhibition of Foxm1 reversed the tumor-promoting effects induced by RNF112 knockdown.
Conclusions:
RNF112 functions as a tumor suppressor in cervical cancer. By promoting Foxm1 ubiquitination, RNF112 inhibits tumor proliferation and alleviates immunosuppression, thereby protecting against oxidative stress-induced mitochondrial dysfunction and ferroptosis in T lymphocytes.
Insights
Ring finger protein 112 (RNF112) acts as a tumor suppressor in cervical cancer by inhibiting proliferation and immune evasion. Low RNF112 levels correlate with poor prognosis, highlighting its clinical significance.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Cervical cancer is a major global health concern for women.
- Molecular mechanisms of cervical cancer progression and immune evasion require further clarification.
- The role of ring finger protein 112 (RNF112) in cervical cancer is not well understood.
Purpose of the Study:
- To investigate the expression profile of RNF112 in cervical cancer.
- To determine the clinical significance of RNF112 in cervical cancer prognosis.
- To elucidate the molecular mechanisms by which RNF112 influences tumor proliferation and immune responses.
Main Methods:
- Quantitative PCR and Western blotting to analyze RNF112 expression in patient tissues and cell lines.
- In vitro and in vivo (xenograft mouse model) experiments to assess RNF112's effect on tumor growth.
- Co-culture systems and molecular analyses to evaluate RNF112's impact on T lymphocytes, oxidative stress, mitochondrial function, ferroptosis, and Foxm1 ubiquitination.
Main Results:
- RNF112 expression was significantly downregulated in cervical cancer tissues and cell lines.
- Low RNF112 expression correlated with poorer patient prognosis.
- RNF112 suppressed tumor growth, alleviated immunosuppression in the tumor microenvironment, reduced oxidative stress and ferroptosis in T lymphocytes, and promoted Foxm1 ubiquitination and degradation.
Conclusions:
- RNF112 functions as a tumor suppressor in cervical cancer.
- RNF112 inhibits cervical cancer proliferation and immune evasion by promoting Foxm1 ubiquitination.
- RNF112 protects T lymphocytes from oxidative stress, mitochondrial dysfunction, and ferroptosis.
Related Concept Videos
Abnormal Proliferation
Experimental RNAi
MicroRNAs
MicroRNAs
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-kB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...