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.
2 months ago
Journal
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ERBB4 (erb-b2 receptor tyrosine kinase 4) • BCL11B (BAF Chromatin Remodeling Complex Subunit BCL11B) • WNT7A (Wnt Family Member 7A) • CALB2 (Calbindin 2) • SLC1A2 (Solute Carrier Family 1 Member 2)
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.
9 months ago
Journal
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FOSL1 (FOS Like 1) • GLI2 (GLI Family Zinc Finger 2) • CALB2 (Calbindin 2) • WTAP (WT1 Associated Protein)
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.
1 year ago
Journal
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LDHA (Lactate dehydrogenase A) • CALB2 (Calbindin 2) • GLUD2 (Glutamate Dehydrogenase 2) • SLC4A1 (Solute Carrier Family 4 Member 1)
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.
1 year ago
Journal
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CALB2 (Calbindin 2) • FABP4 (Fatty Acid Binding Protein 4)
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.
COADREADx provides uncertainty measures for its predictions and needs clinical validation. It has been deployed for experimental non-commercial use at: https://apalanialab.shinyapps.io/coadreadx/.
over 1 year ago
Journal
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DKK1 (dickkopf WNT signaling pathway inhibitor 1) • CXCL13 (Chemokine (C-X-C motif) ligand 13) • HOTAIR (HOX Transcript Antisense RNA) • CDH3 (Cadherin 3) • TINCR (TINCR Ubiquitin Domain Containing) • CALB2 (Calbindin 2) • HSP90AB1 (Heat Shock Protein 90 Alpha Family Class B Member 1) • IGFBP1 (Insulin Like Growth Factor Binding Protein 1) • ESM1 (Endothelial Cell Specific Molecule 1)
A Wnt activator, CHIR99021, was pivotal in MPC maturation to CALB2+ mesothelial cells, while BMP4 or FGF2 was limited. Our results demonstrated central pathways critical for mesothelial cell behaviors.
These findings identify CALB2 as a key regulator of inflammatory reprogramming to promote PDAC metastatic progression. Combination therapy with αCXCL14 monoclonal antibody and gemcitabine emerges as a promising strategy to suppress distant metastasis and improve survival outcomes in PDAC with CALB2 overexpression.