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Ferredoxin 1: a gatekeeper in halting lung adenocarcinoma progression through activation of the GPRIN2 signaling
Ming Liu1,2,3, Shaoxian Wu1, Haoyu Wu1
1Department of Tumor Biological Diagnosis and Treatment Center, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, Jiangsu, China.
Background:
Lung adenocarcinoma (LUAD) is a highly lethal form of lung cancer. Despite advancements in treatments, managing LUAD is still challenging due to its aggressive behavior. Recent studies indicate that various molecular pathways, including the dysregulation of ferredoxin 1 (FDX1), play roles in LUAD progression. FDX1, a crucial protein in cellular redox reactions and energy metabolism, has been linked to several cancers. However, its exact role in the development of LUAD is not yet fully understood.
Methods:
We investigated the role of ferredoxin 1 (FDX1) in LUAD progression through analysis of its expression in LUAD tissues and its impact on patient survival. Functional assays were performed to assess the effects of FDX1 overexpression on LUAD cell proliferation, migration, and invasion. A xenograft model was employed to evaluate the tumorigenesis potential of LUAD cells with FDX1 overexpression. Mechanistic insights into FDX1 regulation were gained through depletion experiments targeting the G protein-regulated inducer of neurite outgrowth 2 (GPRIN2)/PI3K signaling pathway.
Results:
FDX1 expression was down-regulated in LUAD tissues, correlating with shorter patient survival. Overexpression of FDX1 suppressed LUAD cell proliferation, migration, and invasion in vitro, and inhibited tumorigenesis in vivo. Mechanistically, the GPRIN2/PI3K signaling pathway was implicated in FDX1 regulation, as depletion of GPRIN2 reversed the effects of FDX1 overexpression on cellular functions.
Conclusions:
Our findings highlight FDX1 as a potential tumor suppressor in LUAD, acting through modulation of the GPRIN2/PI3K signaling pathway. These results suggest FDX1 as a promising therapeutic target for LUAD treatment, warranting further investigation into its clinical relevance.
Insights
Ferredoxin 1 (FDX1) acts as a tumor suppressor in lung adenocarcinoma (LUAD), inhibiting cancer cell growth. FDX1 may be a therapeutic target for LUAD treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Lung adenocarcinoma (LUAD) is an aggressive cancer with challenging management.
- Ferredoxin 1 (FDX1) is implicated in cancer progression, but its role in LUAD is unclear.
Purpose of the Study:
- To investigate the role of FDX1 in LUAD progression and patient survival.
- To elucidate the molecular mechanisms underlying FDX1 regulation in LUAD.
Main Methods:
- Analyzed FDX1 expression in LUAD tissues and correlated with patient survival.
- Performed functional assays to assess FDX1's impact on LUAD cell proliferation, migration, and invasion.
- Utilized a xenograft model and GPRIN2/PI3K pathway analysis to explore FDX1 regulation.
Main Results:
- FDX1 expression was decreased in LUAD tissues, linked to poorer survival.
- FDX1 overexpression inhibited LUAD cell proliferation, migration, invasion, and tumorigenesis.
- The GPRIN2/PI3K pathway mediated FDX1's effects on LUAD cell functions.
Conclusions:
- FDX1 functions as a tumor suppressor in LUAD by regulating the GPRIN2/PI3K pathway.
- FDX1 represents a potential therapeutic target for lung adenocarcinoma treatment.
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