ELF5 (E74 Like ETS Transcription Factor 5)

This study substantially advances our understanding of the etiology of LUAD in East Asia and could be useful in developing translational applications.

Mice lacking each of these molecules have impaired alveologenesis during pregnancy. Finally, several data seem to suggest a strong functional relationship between the onco suppressor gene BRCA1 (Breast cancer gene 1) and the reversible adipo-epithelial transdifferentiation phenomenon opening new avenues for future studies in the connection between pinking and breast cancer.

We developed a novel approach for selecting cancer-specific normal-invariant genes from relevant gene expression data. Although we believe that tissue-specific reactivation of embryonic genes might explain the cancer-specific differences of MSI CRC and EC, further studies are needed for validation.

Further studies are required to elucidate the molecular mechanisms and assess the clinical potential of these findings. These findings demonstrate the critical role of NLRP7 and associated genes in LUAD metastasis and suggest that AH-6809 holds promise as a potential therapeutic agent for brain-metastatic LUAD.

Transcription factor analyses identify loss of ELF5 and gain of AP-1 sites in these epigenetically primed regions; in vivo experiments further implicate AP-1 and Wnt10a as strong promoters of Brca1-related breast cancer. These findings reveal a previously unappreciated epigenetic effect of Brca1 haploinsufficiency in accelerating tumorigenesis, advancing our mechanistic understanding and informing potential therapeutic strategies.

Conclusion  RNA sequencing is a viable and informative approach for genomic profiling of archival SNUC samples. Both SR-SNUC and SD-SNUC were noted to have distinct genetic profiles underlying the molecular classification of these diseases.

This review focuses on the role of ELF5 in normal breast development, its altered expression throughout aging, and its implications in cancer. It discusses the lineage-specific expression of ELF5, its regulatory mechanisms, and its potential as a biomarker for breast-specific biological age and cancer risk.

These results indicate that KLF5 can downregulate the EMT process of HeLa cells by decreasing the expression of the SNAI1 gene, thereby inhibiting the migration and invasion of HeLa cervical cancer cells.

Our findings suggest that ELF5 promoter methylation in circulating DNA could serve as a potential non-invasive prognostic molecular marker in breast cancer patients. However, further studies are warranted to evaluate its diagnostic value.

(1) This study found a statistical difference between HPV integration and the occurrence of VaIN; (2) HPV integration may provide a new clinical predictor for VaIN and facilitate risk assessment and stratified management of high-risk patients.

Downregulation of ELF5 due to DNA hypermethylation inhibits RCC development though the USP3/WDTC1axis in RCC.

Knockdown of ELF4 in cancer cells also inhibited M2 macrophage polarization and chemotaxis towards 769-P and 786-O cells. Conclusively, the present findings indicated the clinical significance of ELF4 in ccRCC, and verified its key role in driving cell proliferation, migration and invasion, and promoting M2 macrophage polarization and chemotaxis in ccRCC.