HTRA3 (HtrA Serine Peptidase 3)

This has significant implications for antibiotic discovery pipelines and industrial production, where glucose-rich media are preferred for cost and scalability. Our results position CutRS as a key target for future strain-improvement strategies.

Using this signature, we identified paeoniflorin as a novel FBXO22-dependent BACH1 degrader with anti-invasive activity, and the novel BACH1 target gene HTRA3 as a potential effector of BACH1's pro-migratory effect. In summary, this novel BACH1 signature holds potential as a therapeutically relevant biomarker for identifying lung tumours with elevated BACH1 activity, serves as a powerful platform for discovering anti-invasive BACH1 inhibitors, and provides mechanistic insights into BACH1's role in driving metastasis.

Although the expression of serine proteases of the HtrA family was dependent on tumour type, stage and the presence of metastases, most articles indicated that HtrA1 and HtrA3 expression in tumours was downregulated compared with healthy tissue or cell lines. The expression of HtrA2 was completely study dependent. The limited number of studies on HtrA4 expression made it impossible to draw conclusions about differences in expression between healthy and tumour tissue. The conclusions drawn from the study suggest that HtrA1 and HtrA3 act as tumour suppressors.

The novel seven-gene (CYTH3, ENG, HTRA3, PDZD4, SAMD14, PGF, and PLN) prognostic model showed high predictive efficiency. The TMB analysis based on the seven genes could depict the basic profile of the immune response in HCC, which might be worthy of clinical application.

Results of in vitro experiments indicated that HtrA3 gene knockdown inhibits the proliferation of FaDu and Cal-27 cells while concurrently promoting apoptosis. HtrA3 shows significant potential as both a prognostic marker and a promising therapeutic target for HNSCC, highlighting its relevance and importance in future research and potential clinical applications.

Detailed investigations showed that forkhead box protein 1 (FOXP1), an oncogene in OS progression, downregulated HTRA3 expression and inhibited the transcriptional activity of HTRA3, suggesting that HTRA3 was regulated negatively by FOXP1. In conclusion, our study demonstrates that HTRA3 is a repressor involved in OS development via the PTEN/PI3K/AKT pathway under the modulation of transcription factor FOXP1, and it may provide a therapeutic direction for OS patients.

The combination not only refines target expression cell types (E.g. primary tumor or immune system) but also provide a strong indicator for target GE variability within patients' tumors for improved precision medicine approaches.