ZBTB7A (Zinc finger and BTB domain containing 7A)

As a transcription factor, ZBTB7A promotes lymphangiogenesis and facilitates lymph node metastasis by upregulating the transcription of VEGFA and activating AKT pathway. Collectively, our findings reveal that the USP43/ZBTB7A axis plays a crucial role in promoting lymphatic metastasis of bladder cancer, offering potential therapeutic and preventive strategies for lymph node metastatic bladder cancer.

Our results indicated that interventions targeting ANRIL-shZBTB7A and SREBP inhibitors can effectively disrupt lipid metabolism and impair the invasive and metastatic properties of NPC cells. These findings provide valuable insights into the potential experimental strategies for inhibiting NPC metastasis.

Similar relapse results were obtained in the MRD-negative AAML1531 group, suggesting molecular risk markers can predict outcome and thus be used to stratify therapy in ML-DS. https://clinicaltrials.gov/study/NCT02521493.

ZBTB7A was identified as a key regulator of PTGES3, while interactions among LGALS9, P4HB, and CD44 significantly impacted signaling pathways influencing the tumor microenvironment's immune status. Our findings highlight the potential of LS score-based molecular subtyping to improve treatment strategies for lung adenocarcinoma and emphasize PTGES3's role in new therapeutic development.

Furthermore, treatment with ZBTB7A specific inhibitor Curcumin effectively induced colorectal cancer cell death while reducing CD95 expression. These data indicate that ZBTB7A promotes colon cancer cell growth and survival, suggesting its potential as a therapeutic target for colorectal cancer.

TMED3 promotes the malignant progression of GBM by regulating ZBTB7A. In conclusion, this study reveals that TMED3 promotes GBM development through the regulation of the ZBTB7A signaling axis, providing new insights for targeted therapy of GBM.

However, ZBTB7A mRNA levels were only reduced in human CD34+ hematopoietic stem and progenitor cell-derived erythroblasts. Hydroxyurea can act in erythroid cells to reduce the levels and activity of two direct fetal γ-globin transcriptional repressors with accompanying de-repression of the γ-globin genes and induction of HbF, which may explain the mechanism of action leading to amelioration of symptoms in SCD patients treated with this drug.

Notably, pharmaceutical approaches like hydroxyurea, l-glutamine, voxelotor, and crizanlizumab, in addition to therapeutic techniques like gene therapies like Casgevy and Lyfgenia, signify noteworthy advancements in the management of issues connected to SCD. It has been demonstrated that inhibiting these targets can prevent the silencing of the gene encoding for the formation of γ-chains and, in turn, increase the synthesis of HbF, providing a possible treatment option for SCD symptoms. These approaches could pave the way for innovative, mechanism-driven therapies that address the unmet medical needs of SCD patients.

High expression of ZBTB7A in triple-negative breast cancer is significantly associated with poor response to neoadjuvant chemotherapy. Our work furthers the understanding of KDM5-mediated gene regulation and identifies mediators of sensitivity to KDM5i.

MFGE8 promoted cell proliferation, EMT progress, and tumor growth of gastric cancer by activating the IL-6/JAK/STAT3 signaling.

Notably, the review concludes with a summary of the recent applications of targeting ZBTB7A in clinical treatments through gene silencing, immunotherapy and chemotherapeutic approaches to halt or slow tumor progression. We focus on the functional role and regulatory mechanisms of ZBTB7A in cancer with the goal of providing new insights for the development of more effective cancer therapeutic strategies.

The Cancer Genome Atlas (TCGA) analyses revealed that overall survival is better in patients with high ZBTB7A expression in their tumor tissues. These findings highlight the potential of targeting the ZBTB7A-ZBTB2 interaction as a novel therapeutic strategy to inhibit HIF-1 activity and improve treatment outcomes in hypoxia-related cancers.