CRTAC1 (Cartilage Acidic Protein 1)

Functionally, CRTAC1 inhibits the proliferation, migration, and invasion of LUAD cells both in vitro and in vivo by suppressing integrin/FAK signaling. These findings highlight CRTAC1 as a potential therapeutic target for LUAD, offering new avenues for treatment strategies aimed at reducing tumor progression.

We created a succinct MQRGs risk model to ascertain the LUAD patient's prognosis, potentially offering a novel method for diagnosing and treating this condition.

The gene expressions identified were also altered in thyroid tumors induced by an iodine-deficient diet. These long-term changes in thyroid gene expression caused by neonatal irradiation may be involved in the increased risk of thyroid carcinogenesis.

This work proposed a prognostic tool based on the LLPS-related gene signature to offer prospective and effective biomarkers for lung adenocarcinoma prognosis.

High expression of CRTAC1 in GC tissues affects immunotherapeutic efficacy and prognosis of the patients, possibly by promoting epithelial-mesenchymal transition via modulating tumor mutational load, tumor microenvironment, and the PI3K/AKT signaling pathway.

In the CRTAC1 gene (g.4,203T>C, g.5,348T>G, g.122,451T>C), the mutant CC genotype significantly increased milk fat content, while the heterozygous TG genotype significantly increased lactose content (p G, g.232,922G>C, g.4,203T>C, g.5,348T>G, and g.122,451T>C significantly elevated the lactose, milk fat, and TS content in Gannan yak milk, providing potential molecular marker candidates for improving Gannan yak milk quality.

Upregulation of CRTAC1 significantly inhibited LUAD cell proliferation, invasion, and migration in cellular experiments. CRTAC1 has the potential to serve as a diagnostic and prognostic biomarker in LUAD.

CRTAC1 may participate in progression of UC and serve as a prognostic marker for metastasis. Low CRTAC1 expression was significantly associated with aggressive UC characteristics and worse clinical outcomes. The inclusion of CRTAC1 immunoexpression in the standard pathological variables may optimize the risk stratification of patients.

Taken together, the present results indicate that CRTAC1 overexpression increases the chemosensitivity of NSCLC to cisplatin treatment by inducing Ca-dependent Akt1 degradation and apoptosis, suggesting the potential of CRTAC1 as a biomarker for predicting cisplatin chemosensitivity. Our results further reveal that modulating the expression of CRTAC1 could be a new strategy for increasing the efficacy of cisplatin in chemotherapy of NSCLC patients.