CALB2 (Calbindin 2)

Notably, CALB2 knockdown significantly sensitized CCA tumors to gemcitabine plus radiotherapy, an effect attenuated by KRT7 overexpression. These findings define a novel H3K4 methylation/CALB2/calcium/NF-κB/KRT7/PD-L1 signaling axis that drives immune suppression and therapy resistance in CCA, highlighting its potential as a multi-target strategy for combined immunotherapy and chemoradiotherapy.

Our results uncover novel candidate biomarkers for response to immunotherapy prediction and highlight molecular profiles that could support guided treatment approaches. The predictive models derived at present have the potential to be implemented in clinical practice for decision-making in CRC management.

This multiomics integration reveals a serotonylation-hallmark gene signature that represents microenvironmental characteristics, such as matrix stiffness, stromal density, and immune infiltration, that are pertinent to ultrasound-based CRC therapy. These biomarkers could direct patient classification for radiopharmaceutical, immunotherapy, and ultrasound-enhanced medication delivery. This work supports future clinical trial stratification frameworks and offers a mechanistic basis for precision ultrasound oncology.

Expression analysis indicated that CPS1 and CALB2 were downregulated in NSCLC samples, whereas CDH17, NIPAL4, SOX2, and KREMEN2 were upregulated. The genes CPS1, CDH17, NIPAL4, SOX2, CALB2, and KREMEN2 were identified as prognostic biomarkers in NSCLC, providing insights into their potential roles in disease progression and therapeutic targeting.

These findings advance the concept of 'differentiation therapy' as a promising intervention to reduce phenotypic plasticity and malignancy in pHGG ecosystems. While these are early in vitro findings, the potential ability to steer and control glioma cells toward stable, less malignant fates offers promising translational potential for patient-centered targeted therapies.

Mechanistically, CALB2 overexpression inhibited NP development by activating the cyclic adenosine monophosphate/cAMP response element-binding protein (cAMP/CREB) signaling pathway. CALB2 overexpression inhibits oxidative stress and promotes microglia transition from M1 to M2 phenotype by activating the cAMP/CREB pathway, which in turn attenuates NP.

WTAP knockdown restrained the growth and metastasis of PAAD in nude mice via the FOSL1/CALB2 axis. In conclusion, WTAP increased the m6A level of FOSL1, activated CALB2 transcription, and promoted M2 polarization of macrophages, thereby promoting the growth and metastasis of PAAD.

Cytoplasmic HuR expression increases the chemoresistance and postoperative recurrence risk of pleural mesothelioma, making it a potential biomarker for predicting therapeutic prognosis. However, the mechanism of HuR transfer to the cytoplasm remains unclear for therapeutic application.

This subset of patients may potentially respond well to immune checkpoint inhibitor therapy. MIRPS may be used as a novel prognostic tool for CC and have potential value for immunotherapy response prediction.

In addition, PI propelled the metastasis of GH3 cells in vivo, and elevated the expression of PITPNM1, POU1F1, C2orf15 and LDHA. These results suggested that elevated serum PI might contribute to the proliferation and invasion of pituitary adenoma by regulating the expression of PITPNM1/AKT/ERK/POU1F1 axis.

This comprehensive analysis identified a lactylation-related signature with significant prognostic and therapeutic implications for COAD. The findings highlight the importance of lactylation in COAD biology and offer novel insights for developing personalized treatment strategies, potentially improving patient outcomes in this prevalent malignancy.

Next-generation sequencing revealed multiple differential features between SF- MPNST, D-MPNST, SCM, and DM, including tumor mutation burden, mutational signatures, and differentially expressed genes. These findings help advance our understanding of disease pathogenesis and improve diagnostic modalities.