Integrinβ-1 in disorders and cancers: molecular mechanisms and therapeutic targets

Abstract

Integrinβ-1 (ITGB1) is a crucial member of the transmembrane glycoprotein signaling receptor family and is also central to the integrin family. It forms heterodimers with other ligands, participates in intracellular signaling and controls a variety of cellular processes, such as angiogenesis and the growth of neurons; because of its role in bidirectional signaling regulation both inside and outside the membrane, ITGB1 must interact with a multitude of substances, so a variety of interfering factors can affect ITGB1 and lead to changes in its function. Over the past 20 years, many studies have confirmed a clear causal relationship between ITGB1 dysregulation and cancer development and progression in a wide range of benign diseases and solid tumor types, which may imply that ITGB1 is a prognostic biomarker and a therapeutic target for cancer treatment that warrants further investigation. This review summarizes the biological roles of ITGB1 in benign diseases and cancers, and compiles the current status of ITGB1 function and therapy in various aspects of tumorigenesis and progression. Finally, future research directions and application prospects of ITGB1 are suggested.

Identification of New Chemoresistance-Associated Genes in Triple-Negative Breast Cancer by Single-Cell Transcriptomic Analysis

“…In doxorubicin-resistant cells, the mesenchymal gene signature in cluster 1 (depicted in orange in Figure 5c) also suggested an activated EMT process that probably mediates increased drug resistance. This may be linked to the overexpression of ITGB1 in this cluster (Figure 5d), a multi-functional cell adhesion molecule that is known to trigger EMT and promote drug resistance in cancer cells [42], suggesting that integrin signaling inhibitors could also disrupt mesenchymal features and sensitize cells to doxorubicin. The presence of the transcription factor STAT1 (Signal transducer and activator of transcription 1) and the enzyme MMP2 (matrix metallopeptidase 2) in cluster 2 (depicted in green in Figure 5c) implied roles for inflammation and extracellular matrix remodeling, respectively, in these cells, two processes that are interlinked and known to support cancer progression [43] and drug resistance [44].…”

Hypoglycemic Activity of Rice Resistant-Starch Metabolites: A Mechanistic Network Pharmacology and In Vitro Approach

“…The interaction between bile acids and ITGB1 protein was mainly achieved by linking to Arg420, Leu419, Glu171, and Arg106. The Arg420 of ITGB1 was able to form a salt-bridge interaction with the Asp residue in the Arg-Gly-Asp sequence, facilitating their binding [54]. Similarly, ITGAV is a member of the integrin family that facilitates cell adhesion to the extracellular matrix by recognizing ligands containing the RGD sequence, and Arg and Asp residues might play an important role in this process.…”