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Mechanisms of Small Molecule Inhibitors Targeting Cancer
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Mechanisms of Small Molecule Inhibitors Targeting Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (20 March 2025) | Viewed by 4026

Special Issue Editor

Dr. Silvia Martina Ferrari

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy
Interests: chemokines; autoimmune thyroid disorders; thyroid cancer; primary cell cultures; autoimmunity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Thyroid cancer (TC) is a highly diffuse endocrine tumor, with a rising incidence in the last 20 years. Besides traditional treatment strategies, a better understanding of the genomic landscape of TC could help clinicians to develop more tailored therapy for patients. 

Tyrosine kinase receptors are involved in cancer cell proliferation and angiogenesis. The antiangiogenic multi-targeted kinase inhibitors sorafenib, lenvatinib, and cabozantinib have been approved to treat aggressive radioactive iodine (RAI)-resistant papillary TC or follicular TC. Other compounds have been introduced for TC patients that harbor specific mutations. For example, selpercatinib and pralsetinib inhibit mutant RET in medullary TC, and block RET fusion protein-mediated signaling in papillary TC; entrectinib and larotrectinib can be used in patients with progressive RAI-resistant TC harboring TRK fusion proteins; FDA authorized the association of dabrafenib (BRAFV600E inhibitor) and trametinib (MEK inhibitor) in BRAFV600E-mutated ATC. 

Additional studies are needed to identify the potential effective targeted therapies for aggressive TCs, according to their molecular characterization.

Dr. Silvia Martina Ferrari
Guest Editor

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Published Papers (3 papers)

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Research

16 pages, 6902 KiB  
Article
A Novel Rexinoid Agonist, UAB116, Decreases Metastatic Phenotype in Hepatoblastoma by Inhibiting the Wnt/β-Catenin Pathway via Upregulation of TRIM29
by Swatika Butey, Morgan L. Brown, Janet R. Julson, Raoud Marayati, Venkatram R. Atigadda, Maryam G. Shaikh, Nazia Nazam, Colin H. Quinn, Sorina Shirley, Laura L. Stafman and Elizabeth A. Beierle
Int. J. Mol. Sci. 2025, 26(9), 3933; https://doi.org/10.3390/ijms26093933 - 22 Apr 2025
Viewed by 244
Abstract
Hepatoblastoma (HB) is the most common pediatric primary liver tumor. About 20% of affected children have pulmonary metastasis at presentation. Survival rates for these children are dismal, not exceeding 25%. To study this subset of patients, we sequenced a metastatic HB cell line, [...] Read more.
Hepatoblastoma (HB) is the most common pediatric primary liver tumor. About 20% of affected children have pulmonary metastasis at presentation. Survival rates for these children are dismal, not exceeding 25%. To study this subset of patients, we sequenced a metastatic HB cell line, HLM_2, and identified downregulation of the Liver X Receptor (LXR)/Retinoid X Receptor (RXR) pathway. LXR/RXRs function as transcriptional regulators that influence genes implicated in HB development, including the Wnt/β-catenin signaling pathway. We assessed the effects of a novel LXR/RXR agonist, UAB116, on metastatic HB, hypothesizing that this compound would affect genes governing the Wnt/β-catenin pathway, decreasing the metastatic phenotype of HLM_2 metastatic HB cells. We evaluated its effects on viability, proliferation, stemness, clonogenicity, and motility, and performed RNA sequencing to study differential gene regulation. Treatment with UAB116 for 72 h decreased HLM_2 proliferation, stemness, clonogenicity, and invasion. RNA sequencing identified an eight-fold increase in TRIM29, a gene known to inhibit β-catenin, in cells treated with UAB116. Administration of the LXR/RXR agonist, UAB116, reduces proliferation, stemness, and invasiveness of metastatic HB cells, potentially by upregulation of TRIM29, a known modulator of the Wnt/β-catenin pathway, providing support for further exploration of LXR/RXR agonism as a therapeutic strategy for metastatic HB. Full article
(This article belongs to the Special Issue Mechanisms of Small Molecule Inhibitors Targeting Cancer)
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17 pages, 2233 KiB  
Article
Antineoplastic Effect of ALK Inhibitor Crizotinib in Primary Human Anaplastic Thyroid Cancer Cells with STRN–ALK Fusion In Vitro
by Silvia Martina Ferrari, Francesca Ragusa, Giusy Elia, Valeria Mazzi, Eugenia Balestri, Chiara Botrini, Licia Rugani, Armando Patrizio, Simona Piaggi, Concettina La Motta, Salvatore Ulisse, Camilla Virili, Alessandro Antonelli and Poupak Fallahi
Int. J. Mol. Sci. 2024, 25(12), 6734; https://doi.org/10.3390/ijms25126734 - 19 Jun 2024
Cited by 2 | Viewed by 1466
Abstract
Anaplastic thyroid cancer (ATC) is one of the deadliest human cancers and represents <2% of thyroid carcinomas. A therapeutic target for ATC is represented by anaplastic lymphoma kinase (ALK) rearrangements, involved in tumor growth. Crizotinib is an oral small-molecule tyrosine kinase inhibitor of [...] Read more.
Anaplastic thyroid cancer (ATC) is one of the deadliest human cancers and represents <2% of thyroid carcinomas. A therapeutic target for ATC is represented by anaplastic lymphoma kinase (ALK) rearrangements, involved in tumor growth. Crizotinib is an oral small-molecule tyrosine kinase inhibitor of the ALK, MET, and ROS1 kinases, approved in ALK-positive non-small cell lung cancer. Until now, the effect of crizotinib in “primary human ATC cells” (pATCs) with transforming striatin (STRN)–ALK fusion has not been reported in the literature. In this study, we aimed to obtain pATCs with STRN–ALK in vitro and evaluate the in vitro antineoplastic action of crizotinib. Thyroid surgical samples were obtained from 12 ATC patients and 6 controls (who had undergone parathyroidectomy). A total of 10/12 pATC cultures were obtained, 2 of which with transforming STRN–ALK fusion (17%). Crizotinib inhibited proliferation, migration, and invasion and increased apoptosis in 3/10 pATC cultures (2 of which with/1 without STRN–ALK), particularly in those with STRN–ALK. Moreover, crizotinib significantly inhibited the proliferation of AF cells (a continuous cell line obtained from primary ATC cells). In conclusion, the antineoplastic activity of crizotinib has been shown in human pATCs (with STRN–ALK) in preclinical studies in vitro, opening the way to future clinical evaluation in these patients. Full article
(This article belongs to the Special Issue Mechanisms of Small Molecule Inhibitors Targeting Cancer)
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16 pages, 2842 KiB  
Article
The Bifunctional Effects of Lactoferrin (LFcinB11) in Inhibiting Neural Cell Adhesive Molecule (NCAM) Polysialylation and the Release of Neutrophil Extracellular Traps (NETs)
by Bo Lu, Si-Ming Liao, Shi-Jie Liang, Li-Xin Peng, Jian-Xiu Li, Xue-Hui Liu, Ri-Bo Huang and Guo-Ping Zhou
Int. J. Mol. Sci. 2024, 25(9), 4641; https://doi.org/10.3390/ijms25094641 - 24 Apr 2024
Cited by 1 | Viewed by 1597
Abstract
The expression of polysialic acid (polySia) on the neuronal cell adhesion molecule (NCAM) is called NCAM-polysialylation, which is strongly related to the migration and invasion of tumor cells and aggressive clinical status. Thus, it is important to select a proper drug to block [...] Read more.
The expression of polysialic acid (polySia) on the neuronal cell adhesion molecule (NCAM) is called NCAM-polysialylation, which is strongly related to the migration and invasion of tumor cells and aggressive clinical status. Thus, it is important to select a proper drug to block tumor cell migration during clinical treatment. In this study, we proposed that lactoferrin (LFcinB11) may be a better candidate for inhibiting NCAM polysialylation when compared with CMP and low-molecular-weight heparin (LMWH), which were determined based on our NMR studies. Furthermore, neutrophil extracellular traps (NETs) represent the most dramatic stage in the cell death process, and the release of NETs is related to the pathogenesis of autoimmune and inflammatory disorders, with proposed involvement in glomerulonephritis, chronic lung disease, sepsis, and vascular disorders. In this study, the molecular mechanisms involved in the inhibition of NET release using LFcinB11 as an inhibitor were also determined. Based on these results, LFcinB11 is proposed as being a bifunctional inhibitor for inhibiting both NCAM polysialylation and the release of NETs. Full article
(This article belongs to the Special Issue Mechanisms of Small Molecule Inhibitors Targeting Cancer)
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