PPIA (Peptidylprolyl Isomerase A)

Conclusions This study establishes BSG/CD147 upregulation as an early molecular event in hepatocarcinogenesis that integrates hepatocyte dedifferentiation, microenvironmental signaling, and tumor progression. Strong and specific expression in small lesions < 2 cm underscores potential as a precision biomarker and imaging target for early HCC detection, risk stratification, and therapeutic development.

Sdcbp and Rpl22 were most abundantly expressed in Microglia, and Ppia in Oligodendrocytes, while Sec61g exhibited lower overall expression, all showing high activity in immune metabolic pathways. Bioinformatics analysis and experimental verification indicate that Sdcbp, Ppia, and Sec61g are associated with ferroptosis and immune infiltration in IS, and hold promise as therapeutic targets for IS treatment.

A prognosis model based on fatty acid metabolism can serve as an effective tool for assessing the prognosis of LUAD patients. Due to incomplete clinical information in some datasets, comprehensive subgroup analyses could not be performed.

This study highlights the novelty of our pipeline in integrating RNA-seq data to identify robust intercellular communication networks in AD. By prioritizing consistent interactions across datasets, we provide insights into AD pathology that inform experimental validation and therapeutic development.

By applying multiplex immunofluorescence for selected markers, we validated the presence of the separate cell entities. Our findings provide deeper insights into the biology of PTBTs, which may be beneficial for advancing the diagnosis and therapy of PTBTs.

Cell-cell interaction analysis showed that the increased CD44-TYROBP-mediated and decreased PPIA-BSG and APP-SORL1-mediated cell communication between tumor cells and other cells.Specifically, CD8+ resident memory T cells emerged as pivotal regulators in LM of PTC, primarily through the expression of MHC-I, CD99 and LCK. This study provides new insights into the heterogeneity of PTC and the basis for LM in PTC, which might provide potential therapeutic targets in future treatment.

This study indicated that different risk score groups exhibited different tumor mutation burden, immune microenvironment cell infiltration, immune response, differentially expressed genes, functional characteristics, correlations with immune checkpoint genes, and drug sensitivity. We established a novel ferroptosis-related oxidative stress gene-related model that possesses potential predictive value for prognosis of patients with LUAD, immunotherapy response, and chemotherapeutic drug sensitivity, and indicated its potential applicability in clinical practice.

This study establishes PLK2 as a key regulator of glycolysis and immune imbalance in PCOS, highlighting its pivotal role in the metabolic-immune crosstalk within the ovarian microenvironment. These findings suggest that targeting PLK2 may be a potential therapeutic strategy for alleviating glycolytic dysregulation and chronic inflammation in PCOS.

CPNE1 is linked to poor prognosis in hepatocellular carcinoma (HCC) and proposes the SNHG6/hsa-miR-101-3p/CPNE1 regulatory axis. The study investigates the role of CPNE1 in modulating the immune microenvironment of liver cancer and suggests that it may serve as a biomarker for poor prognosis in HCC patients.

Given the significant impact of hypoxia on T cell metabolism and function in the tumor microenvironment, selecting reliable reference genes is crucial for accurate gene expression analysis. Our findings will be valuable for future studies investigating hypoxia-driven metabolic reprogramming in immune cells, ultimately contributing to a better understanding of T cell responses in cancer immunotherapy.

Virtual screening identified arbutin and imatinib mesylate as candidate CHP1-targeting compounds. These findings establish CHP1 downregulation as a novel molecular feature of ccRCC progression and support its utility as a prognostic biomarker.

Strikingly, activating KDM6B expression with paricalcitol or inhibiting the Notch pathway with DAPT effectively counteracted NSUN2-induced osteolytic bone metastasis in vivo. Collectively, our findings underscore the pivotal role of the NSUN2-KDM6B-Notch axis in promoting osteoclast differentiation and bone metastasis in BCa, providing potential therapeutic targets for BCa patients with bone metastasis.