HTRA1 (HtrA Serine Peptidase 1)

Furthermore, HPV E7 could inhibit the secretion of type I IFN from cells, thus leading to persistent viral infection. These findings provide novel insights into the association between HPV infection and mitophagy, and may elucidate the mechanisms underlying persistent HPV infection.1.

Furthermore, utilizing ultra-pH-sensitive nanoparticle imaging and metabolite analysis, we identify regions of acidification, elevated lactate, and enrichment of immunosuppressive (M2-like) macrophages in LUSC tumors. These results demonstrate that TMPRSS11B promotes an acidified and immunosuppressive TME and nominate this enzyme as a therapeutic target in LUSC.

Quantitative real-time polymerase chain reaction (qRT-PCR) validation in a bleomycin-induced mouse model confirmed differential expression of the seven model genes, aligning with transcriptomic predictions. The prognostic signature based on PCD-related genes provides new biomarkers for the prognostic assessment of IPF, and has high predictive accuracy. Additionally, the identified potential drugs offer new directions for the treatment of IPF, laying the foundation for future individualized therapies.

Regarding cognitive frailty, CRP, TNF-α, and GDF15 displayed significant associations with this condition. sTNF-RII and HTRA1, scarcely studied in this context, showed promising and significant associations (specific for cognitive frailty in the case of HTRA1) that justify their inclusion in future research aimed at better understanding the inflammatory mechanisms involved in cognitive frailty.

It may contribute to tumorigenesis through an alternative pathway independent of NF2. Our findings provide a basis for future clinical investigations.

We describe a schwannoma arising in the periportal region in which a novel TANC1::HTRA1 fusion was identified. The identification of this variant expands the range of fusion drivers in schwannoma and offers insight into the pathogenic mechanism of HTRA1 fusions and their utility in molecular diagnosis.

Furthermore, a molecular network comprising four transcription factors and 11 downstream genes was discovered. This newly identified molecular network enhances our understanding of the distinct mechanisms underlying IPF and SCC onset, and provides new insights into preventing SCC complications in patients with IPF.

KLF13 can serve as a tumor promoter in breast cancer by influencing HTRA1 and the Hedgehog signaling pathway.

In contrast, other tumor areas exhibiting high expression of TMPRSS11B together with BSG and SLC16A1 were largely negative for KLF4 expression. Thus, the differential expression of TMPRSS11B adds to metabolic heterogeneity in PDAC and its absence supports the reverse Warburg metabolism in PDAC cells by the enhancement of BSG-supported lactate uptake through SLC16A1 and subsequent phenotype alterations towards greater stemness.

Restoring LATS2 expression in HTRA1-deficient CRC cells decreased EMT and anoikis resistance. Altogether, our findings unveiled the negative regulatory function of HTRA1 in CRC progression through the regulation of the Hippo/YAP1 pathway, and supported HTRA1 as a potential therapeutic target in CRC.

CCL5, CXCL9, CXCL13, and HTRA1 were OS hub genes positively correlate with CD8+ T cell and CD4+ T cell infiltrations. HTRA1 can serve as an underlying biomarker for the prognosis and immunotherapy of OS.

Our results suggested the potential involvement of factors other than NF2 inactivation in tumorigenesis, especially in non-VS. However, further comprehensive molecular analyses are warranted.