GNL3 (G Protein Nucleolar 3)

Knockdown of GNL3 sensitizes HR-proficient breast cancer cells to etoposide or Olaparib treatment. Together, our results reveal that GNL3 SUMOylation is crucial for HR repair and suggest that targeting GNL3 SUMOylation may induce HR deficiency, thereby sensitizing breast cancers to DNA damage-inducing agents.

GNL3L correlates with ESCC malignancy, influencing the MDM2-p53-p21 axis. GNL3L-MDM2 interaction is critical in ESCC progression.

These results strongly indicated that GNL3L has the capability to activate the NF-κB and increase Slug, MMP2, and MMP9 expression, which in turn could stimulate the proliferation, migration, and invasion of lung cancer cells. NF-κB activation and Slug, MMP2, and MMP9 expression enhanced by GNL3L, leading to the promotion of proliferation, migration, and invasion of lung cancer cells, indicating the therapeutic implications and potential significance of these pathways in the progression and invasion of NSCLCs that overexpress GNL3L protein.

GNL3 is key in the progression of LUAD by metiating Wnt/β-catenin axis. Targeting GNL3 may represent a novel therapeutic method for LUAD treatment.

GNL3L enhanced RELA activity, activated NF-κB, promoted AML cell proliferation, resisted apoptosis, and encouraged cytarabine resistance in AML. In conclusion, these data suggest a role for GNL3L in the malignant process of AML and as a promising therapeutic target.

High GNL3L expression significantly contributes to the malignant progression of ESCC. This study further elucidates the mechanisms driving ESCC progression and offers possible insights for more effective diagnosis and treatment strategies.

Moreover, AMPK activity alteration influenced the effect of GNL3L in regulating cell proliferation. Collectively, these findings suggest that GNL3L positively regulates cell proliferation and autophagy in ESCA cells via regulating the AMPK signaling, making itself a promising therapeutic target for ESCA.

The Receiver Operating Characteristics of both genes showed improved area under the curve against sensitivity versus specificity in the pooled samples from three different GSE datasets. Overall, our analysis predicted GNL3 and PA2G4 as prognostic biomarkers of clinical significance in prostate cancer.

The established ESCA prediction model had a strong predictive ability, and GNL3L could significantly affect the proliferation of esophageal cancer cells. In conclusion, GNL3L may serve as an important prognostic biomarker and play an immunomodulatory role in tumors.