CALCR (Calcitonin Receptor 2)

In summary, the current study provides an extensive ceRNA network that highlights novel prognostic biomarkers for stomach adenocarcinoma.

The five-gene signature and RHOV targeting offer translational relevance for risk stratification and therapy. These findings bridge genomic alterations with TME remodeling, advancing precision oncology in LUAD.

CALCR is a crucial factor in GC progression, presenting a potential prognostic marker and therapeutic target. Targeting the CALCR-ANTXR1 axis and AKT pathway offers new avenues for GC treatment.

Our results suggest that Prkd3 modulates proliferation through the regulation of gene expression associated with glucose metabolism (Tnf, Ucp2, Pgam2, Angptl4), calcium homeostasis and transport (Calcr and P2rx7) and microtubule dynamics (Stmn2 and Map10). These candidate processes and associated genes represent potential mechanisms involved in Prkd3-induced proliferation in spontaneously immortalized cells as well as clinical targets in several cancer types.

CALCR serves as a significant prognostic biomarker for LIHC, influencing both molecular pathways and the immune landscape. Its expression is associated with improved survival outcomes and distinct genomic features, positioning it as a potential therapeutic target and predictor of immunotherapy efficacy.

Moreover, a deficiency in CD44 significantly attenuated the promoting role of CALCR on RCC cell proliferation, migration and anti-apoptosis capacities. Collectively, CALCR exacerbates RCC progression via stabilizing CD44, offering a fundamental basis for considering CALCR as a potential therapeutic target for RCC patients.

In sum, TrkA-expressing peripheral neurons positively regulate key aspects of OS progression and sensory neural inhibition appears to disrupt calcitonin receptor signaling (CALCR) and VEGF signaling within the sarcoma microenvironment leading to significantly reduced tumor growth and improved survival. These data suggest that interventions to prevent pathological innervation of osteosarcoma represent a novel adjunctive therapy to improve clinical outcomes and survival.

Specific long non-coding RNAs, instead, have been detected both at reduced levels in patients with multiple myeloma and osteonecrosis, and associated with suppression of osteoblast differentiation, with consequences in the progression of mandible lesions. Among non-coding genic material, circular RNAs have the capability to modify the expression of specific mRNAs responsible for the inhibition of bisphosphonates activity on osteoclastogenesis.

Tumor sections showed increased apoptosis and a decrease in Ki-67 and HIF-1α. These data suggest that in osteosarcoma cells with altered p53, p63, and p73 and a high glycolytic function, Pramlintide therapy can modulate metabolic programming and inhibit tumor growth.