SENP2 (SUMO Specific Peptidase 2)

USP44-SENP2 axis is a pivotal factor in the progression of ESCC, and provides potential therapeutic targets for ESCC patients.

Finally, we performed virtual screening of Food and Drug Administration-approved drugs against SENP2, followed by re-docking analysis and identified four of the most promising candidates. Collectively, our findings characterized SENP2 as a novel prognostic biomarker and a promising therapeutic target in DLBCL.

The authors have stated their consent to the retraction. The authors disagree with the retraction as they have stated they do not agree that image elements were duplicated in Figure 2E.

NSC632839 was an antiproliferative agent in PCa cells at low doses. Therefore, NSC632839 is a strong drug candidate requiring further studies.

The prognostic and immunogenetic value of SENP1 and SENP5 in HCC was demonstrated in this study. Therefore, these two genes have the potential to function as separate prognostic biomarkers and offer promise as immunotherapeutic targets in the fight against HCC.

Finally, miR-145-5p inhibits SENP2 transcription, enhances ERK2 SUMOylation, and ultimately suppresses the progression of breast cancer. These revelations suggest evolving ideas for the miR-145-5p-SENP2 axis in therapeutic intervention, thus heralding transformative prospects for the clinical management of breast cancer.

Consistently, metastatic head and neck cancer cells that do not respond to the mitosis-differentiation checkpoint were resistant to depletion of SENP2. Our results identify SENP2 as a novel regulator of the epithelial mitosis-differentiation checkpoint and a potential biomarker in epithelial cancer.

These data suggest that autocrine VEGF-B mediates a signal to coordinate lipid synthesis and mitochondrial fitness with T cell activation for survival and immune response. Moreover, autocrine VEGF-B signaling in T cells provides a therapeutic target against infection and tumors as well as an avenue for the treatment of autoimmune diseases.

SENP2 promotes ESCC proliferation and enhances fatty acid uptake and oxidation. High expression of SENP2 may be a poor prognostic biomarker for ESCC patients.

Furthermore, miR-629-5p was found to modulate the SENP2/PI3K/AKT/mTOR pathway, impacting IM resistance in CML cells. EVs from IM-resistant CML cells alter the expression of miR-629-5p in sensitive cells, activating the SENP2/PI3K/AKT/mTOR pathway and leading to IM resistance.

In this study, we performed transcriptome screening of peripheral blood plasma obtainedfrom 17 patients before and after receiving combined etoposide and platinum treatment...Moreover, network analysis identifed PRICKLE3, TNFSFI0, ACSLl and EP300 as potential contributors to primary resistance, with SNWl, SENP2 and SMNDCl emerging assignificant factors in acquired resistance, providing valuable insights into chemotherapy resistancein SCLC. These findings offer valuable insights for understanding chemotherapy resistance and related gene signatures in SCLC, which could help further biological validation studies.

This condition leads to the instability of downstream target p21 in accelerating the G1/S cell cycle transition and suggests SENP2 as a promising therapeutic target for lung cancer in the future. Specifically, astragaloside IV, an active ingredient of Jinfukang Oral Liquid (JOL, a clinical combination antilung cancer drug approved by the National Food and Drug Administration (FDA) of China), can repress lung cancer-cell growth via the SENP2-NDR2-p21 axis, which provides new insights into the molecular mechanism of JOL for lung cancer treatment.