Exploring the potential of myo-inositol in thyroid disease management: focus on thyroid cancer diagnosis and therapy

Abstract

Thyroid cancer (TC) is a malignancy that is increasing in prevalence on a global scale, necessitating the development of innovative approaches for both diagnosis and treatment. Myo-inositol (MI) plays a crucial role in a wide range of physiological and pathological functions within human cells. To date, studies have investigated the function of MI in thyroid physiology as well as its potential therapeutic benefits for hypothyroidism and autoimmune thyroiditis. However, research in the field of TC is very restricted. Metabolomics studies have highlighted the promising diagnostic capabilities of MI, recognizing it as a metabolic biomarker for identifying thyroid tumors. Furthermore, MI can influence therapeutic characteristics by modulating key cellular pathways involved in TC. This review evaluates the potential application of MI as a naturally occurring compound in the management of thyroid diseases, including hypothyroidism, autoimmune thyroiditis, and especially TC. The limited number of studies conducted in the field of TC emphasizes the critical need for future research to comprehend the multifaceted role of MI in TC. A significant amount of research and clinical trials is necessary to understand the role of MI in the pathology of TC, its diagnostic and therapeutic potential, and to pave the way for personalized medicine strategies in managing this intricate disease.

Keywords: biomarker; cancer diagnosis; metabolomics; myoinositol; thyroid carcinoma; thyroid nodule.

Figure 1

Illustration of the chair conformations and two-dimensional projections of myo, chiro, and scyllo-inositols.

Figure 2

1H NMR spectrum of myo-inositol. The experimental conditions are as follows: solvent: H₂O; nucleus: 1H; frequency: 600 MHz; sample temperature: 25.0°C, chemical shift reference: DSS. (https://hmdb.ca/).

Figure 3

Myo-inositol de novo biosynthesis from glucose-6-phosphate. The process of glucose-6-phosphate to myo-inositol-1-phosphate conversion follows a series of consecutive reactions that involve the reduction of NAD+ to NADH. Finally, NADH is oxidized to NAD+ when the process is completed. IMPase inositol monophosphatase, MIPS myo-inositol phosphate synthase, NAD nicotinamide adenine dinucleotide, NADH nicotinamide adenine dinucleotide hydrogen, Pi inorganic phosphate.

Figure 4

Supply of myo-inositol needed by the cell from three distinct sources: myo-inositol biosynthesis that includes two distinct biochemical reactions, dephosphorylation of IPs, and absorption from the gastrointestinal tract. The full description is in the text. G6P glucose 6-phosphate, Glu glucose, HK hexokinase, HMIT H+-myo-inositol transporter, IMPase inositol monophosphatase, INPP1 inositol polyphosphate-1-phosphatase, INPP5 inositol polyphosphate-5-phosphatase, IP inositol monophosphate, IP2 inositol bisphosphate, IP3 inositol triphosphate, MI myo-inositol, MIPS myo-inositol phosphate synthase, Na+/K+ ATPase sodium–potassium adenosine triphosphatase, PIP2 phosphatidylinositol bisphosphate, PLC phospholipase C, SMIT1/2 sodium-dependent myo-inositol transporters 1 and 2.

Figure 5

Regulation of thyroid hormone synthesis by two distinct pathways: PIP2 cascade and cAMP cascade. The full description is in the text. AC adenylyl cyclase, ATP adenosine triphosphate, cAMP cyclic adenosine monophosphate, DAG diacylglycerol, GTP guanosine triphosphate, Gαq/11 a subunit of the heterotrimeric G protein, Gαs a subunit of the heterotrimeric G protein, IP3 inositol triphosphate, PI3K phosphoinositide 3-kinase, PIP2 phosphatidylinositol bisphosphate, PIP3 phosphatidylinositol trisphosphate, PKA protein kinase A, PLC phospholipase C, PTEN phosphatase and tensin homolog deleted on chromosome 10, TSH thyroid stimulating hormone, TSHR thyroid stimulating hormone receptor.