ZNF143 (Zinc Finger Protein 143)

This study identified candidate driver fusion genes and suggested new therapeutic targets for HGSOCs.

ZNF143 promotes HCC cell migration and invasion by binding to MEX3C promoter and activating its expression.

Precise analysis using single-cell sorted CD34+/CD38- fractions suggested that ET clone with JAK2-mutated and AML clone with TP53 mutation was derived from the common clone with these mutations. Although further study is required to clarify the biological significance of SMARCC2, UBR4, and ZNF143 mutations during disease progression of ET and AML transformation, the present results demonstrate the possibility of a common initial clone involved in both ET and transformed AML.

Through in vitro and in vivo experiments, we confirmed ZNF143 and EGR1 as downstream transcription factors of CXXC5, mediating its proliferative potential in ovarian cancer. Our findings suggest that the CXXC5-ZNF143/EGR1 axis forms a network driving ovarian cell proliferation and tumorigenesis, and highlight CXXC5 as a potential therapeutic target for ovarian cancer treatment.

LOC644656 recruited ZNF143 to activate E6-AP transcription, promoting cisplatin resistance in CC. In conclusion, LOC644656 positively modulates E6-AP expression via ZNF143-mediated transcriptional activation, contributing to cisplatin resistance in CC.

Downregulation of ZNF143 and KPNA2 can activate the Hippo signalling pathway and reduce YAP/TAZ expression in human glioma cells, thus inducing apoptosis of human glioma cells and weakening their proliferation, migration and invasion. In conclusion, ZNF143 mediates the Hippo/YAP signalling pathway and inhibits the growth and migration of glioma cells by regulating KPNA2.

ZNF143 knockdown blocks lung adenocarcinoma cell migration, which is mediated by ATF1 upregulation. Hence, this study provides a potential therapeutic candidate for the treatment of lung adenocarcinoma.

In order to understand the relationship among ZNF143, gene expression patterns, and noncoding mutations, we adopted an integrative strategy in this study and paid close attention to putative immunological signaling pathways. The immune system-related pathways ErbB, HIF1a, NF-kB, FoxO, JAK-STAT, Wnt, Notch, cell cycle, PI3K-AKT, RAP1, calcium signaling, cell junctions and adhesion, actin cytoskeleton regulation, and cancer pathways are among those that may be significant, according to the overall analysis.

In human BCP-ALL patients treated with CAR-T and blinatumomab, upregulation of NUDT21 mRNA coincided with CD19 loss at disease relapse. Together, these studies identify novel CD19 modulators in human BCP-ALL.

The DNA methyltransferase inhibitor 5-azacytidine (AZA) is a core treatment modality for many patients with MDS/AML, either as a single agent or in combination with other novel agents (e.g., venetoclax). Together, these results indicate a potential role of CTCF in determining the response to AZA by regulating HoxB gene expression in leukemic cells. Given the role of CTCF in forming chromatin loops to regulate gene expression, further studies on changes in chromatin structures within the LSC compartment in AZA responder and non-responder patients will provide deeper insights into how CTCF may determine responsiveness to AZA.

In human B-ALL patients treated with CAR-T and blinatumomab, upregulation of NUDT21 mRNA coincided with CD19 loss at disease relapse. Together, these studies identify new CD19 modulators in human B-ALL.