SAA2 (Serum Amyloid A2)

Furthermore, a combined KIAA1199-SAA2 signature predicts liver metastasis risk in patients. Our findings delineate a KIAA1199-PPARγ/SAA2-Egr1 axis orchestrating the pre-metastatic niche and propose metabolic normalization as a preventative strategy for liver metastasis.

Consistently, supplementing primary HER2-positive tumor cultures with recombinant SAA1, SAA2, or THBS4 peptides enhanced tumor cell proliferation and migration. Together, these findings uncover a mechanism by which fibroblastic mutant p53 promotes mammary tumorigenesis-through upregulating secretory proteins such as SAA1, SAA2, and THBS4 in the stroma, thereby enhancing PI3K/AKT signaling and tumor progression.

In the tumor microenvironment of breast cancer, intercellular communication pairs of different cell types and molecules can exacerbate the development of breast cancer. among them, through the present study, we found that CXCL12-CXCR4 and FGF7-FGFR1 are the most important. Also, most significantly differentially expressed genes including CHRDL1, SCARA5, LYVE1, PI16, and SAA2 seemed to play a critical role in these mechanisms and immune cell infiltration, shaping the TME of BC.

In hepatocyte cultures, LPS increased the expression of HP, SAA2, IL1A, IL1B, IL6, and tumor necrosis factor (TNF) mRNAs (P < 0.05), while D-lactate increased the expression of HP mRNA (P < 0.05), and L-lactate decreased the expression of IL6 mRNA (P < 0.05). Collectively, these in vivo and in vitro findings support the conclusion that both increased concentrations of LPS and D-lactic acid contribute to systemic inflammation during acute ruminal acidosis.

Taken together, the present findings elucidated the B cell-related immunosuppressive landscape in HCC and identified SAA2 as a novel suppressor in HCC, providing a better understanding of the HCC landscape and suggesting a promising therapeutic target for HCC patients.

Co-expression networks and integrative analyses further reinforced these distinctions, uncovering coordinated protein-metabolite modules. Our findings reveal novel, subtype-specific molecular programs in RMS and propose candidate biomarkers and pathways that may guide precision diagnostics and therapeutic targeting in pediatric sarcomas.

The nomogram prognostic prediction model, consisting of ITPKA, PDIA2, SAA2, SHOX2, TREML3P, and ZIC2, is capable of predicting the prognosis of ccRCC patients. Among them, SAA2 promotes the proliferation, migration, and invasion of ccRCC cells.

Some clinical and ultrasonic characteristics of breast cancer were significantly correlated with immune-related genes, such as NR3C2, SAA2, and CXCL9. Further analysis of these genes provides new ideas for the diagnosis and treatment of breast cancer.

These findings establish unique gene signatures for these variants of ST-iCCA, providing potential biomarkers for differential diagnosis, prognosis and targeted therapy. The distinct genetic profiles may also uncover novel therapeutic targets to address the aggressive nature of ST-iCCA.

Plasma IL20RB and SAA2 levels were closely connected with LUAD.

The CRCS2 subtype was in a hypoxic state and was characterized by suppression and exclusion of immune function, which was sensitive to gefitinib, erlotinib, and saracatinib. Our findings highlight the key role of CSCs in shaping the ccRCC tumor microenvironment, crucial for therapy research and clinical guidance. Recognizing tumor stemness helps to predict treatment efficacy, recurrence, and drug resistance, informing treatment strategies and enhancing ccRCC patient outcomes.

MeRIP-qPCR data were concordant with the corresponding MeRIP-seq results in terms of the observed m5C levels. Conjoint analysis identified 190 hyper-up genes characterized by concurrent m5C hypermethylation and up-regulation, alongside 284 hypo-down genes exhibiting both m5C hypomethylation and down-regulation. This study presents the first comprehensive analysis of RNA-m5C modification in BCBM.