Biochemical Signature in Deciphering the Metastasis-Associated Lung Adenocarcinoma Transcript 1/microRNA-145 Axis and Its Molecular Correlation with Nuclear Factor Kappa Beta/Transforming Growth Factor-Beta and Apoptotic Proteins Expression in Colorectal Cancer

Abstract

Colorectal cancer (CRC) is a multifactorial malignancy characterized by complex interactions between oncogenic signaling networks and noncoding RNA regulators. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and microRNA-145 (miR-145) have been recognized as reliable diagnostic biomarkers for cancer. This study evaluates their biochemical interaction, along with their connection to the nuclear factor kappa beta (NF-κβ)/transforming growth factor-beta (TGF-β) signaling pathway and crosstalk with vascular endothelial growth factor (VEGF) and apoptotic markers in CRC. Serum samples were collected from 120 participants, including 90 CRC patients exhibiting a range of tumor grades and anatomical sites, in addition to 30 healthy controls. The expression levels of NF-κB and apoptotic markers were quantified using standardized immunoassays, while the relative expression levels of MALAT1, miR-145, TGF-β, and VEGF were assessed using real-time polymerase chain reaction. Integrative analysis of CRC samples reveals that MALAT1 overexpression correlates with downregulation of miR-145, increased NF-κβ, elevated levels of TGF-β and VEGF, and alterations in apoptotic proteins. Moreover, receiver operating characteristic analysis revealed excellent discriminative power for MALAT1 and miR-145 in distinguishing patients with CRC from healthy controls. These findings suggest that the MALAT1/miR-145 axis serves as a central biochemical node linking inflammatory and fibrotic signaling pathways and apoptotic protein expression in colorectal carcinogenesis. Targeting this regulatory network may offer novel therapeutic opportunities to suppress NF-κβ/TGF-β-driven tumor progression and improve CRC outcomes.