Current Issues in Molecular Biology

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Dear Colleagues,

Recent advances in our understanding of the molecular mechanisms underlying cancer progression have promoted the de novo development of novel small molecules and facilitated drug repositioning to complement contemporary therapeutic approaches to enhance patient survival. Pharmacotherapeutics that target nonredundant pathways in tumor cells required for proliferation, survival and unchecked self-renewal capacity have provided additional strategies to improve standard of care in treating many forms of cancer. Moreover, appreciating the importance of targeting the stromal compartment (e.g., immune cells, fibroblasts, adipocytes) has further exposed therapeutic liabilities in the tumor microenvironment that may present additional options to prevent tumor cell growth and suppress cancer cell resistance to therapeutics. Further identification and elaboration of necessary intracellular pathways and cell–cell signaling mechanisms may inform new pharmacotherapeutic approaches to prevent tumor development, progression, and treatment resistance to build on currently available clinical strategies.

This issue of Current Issues in Molecular Biology is open to both original research articles and review articles focused on the advances in our understanding of actionable mechanisms for pharmacologic exploitation to prevent cancer development and progression. Identifying and elaborating on these mechanisms may provide a path forward in improving patient care and outcomes.

Dr. Peter C. Hart
Guest Editor

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Keywords

cancer
therapeutic resistance
drug tolerance
mechanisms of tumor development
mechanisms of tumor progression

Published Papers (2 papers)

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17 pages, 5527 KiB

Open AccessArticle

The Biological Impact of Some Phosphonic and Phosphinic Acid Derivatives on Human Osteosarcoma

by Zakzak Khaled, Gheorghe Ilia, Claudia Watz, Ioana Macașoi, George Drăghici, Vasile Simulescu, Petru Eugen Merghes, Narcis Ion Varan, Cristina Adriana Dehelean, Lavinia Vlaia and Laurențiu Sima

Curr. Issues Mol. Biol. 2024, 46(5), 4815-4831; https://doi.org/10.3390/cimb46050290 - 15 May 2024

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Abstract

Osteosarcoma malignancy currently represents a major health problem; therefore, the need for new therapy approaches is of great interest. In this regard, the current study aims to evaluate the anti-neoplastic potential of a newly developed phosphinic acid derivative (2-carboxyethylphenylphosphinic acid) and, subsequently, to outline its pharmaco-toxicological profile by employing two different in vitro human cell cultures (keratinocytes—HaCaT—and osteosarcoma SAOS-2 cells), employing different techniques (MTT assay, cell morphology assessment, LDH assay, Hoechst staining and RT-PCR). Additionally, the results obtained are compared with three commercially available phosphorus-containing compounds (P1, P2, P3). The results recorded for the newly developed compound (P4) revealed good biocompatibility (cell viability of 77%) when concentrations up to 5 mM were used on HaCaT cells for 24 h. Also, the HaCaT cultures showed no significant morphological alterations or gene modulation, thus achieving a biosafety profile even superior to some of the commercial products tested herein. Moreover, in terms of anti-osteosarcoma activity, 2-carboxyethylphenylphosphinic acid expressed promising activity on SAOS-2 monolayers, the cells showing viability of only 55%, as well as apoptosis features and important gene expression modulation, especially Bid downregulation. Therefore, the newly developed compound should be considered a promising candidate for further in vitro and in vivo research related to osteosarcoma therapy. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance)

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14 pages, 6895 KiB

Open AccessCommunication

Stemness and Cell Cycle Regulators and Their Modulation by Retinoic Acid in Ewing Sarcoma

by Maria Eduarda Battistella, Natália Hogetop Freire, Bruno Toson, Matheus Dalmolin, Marcelo A. C. Fernandes, Isadora D. Tassinari, Mariane Jaeger, André T. Brunetto, Algemir L. Brunetto, Lauro Gregianin, Caroline Brunetto de Farias and Rafael Roesler

Curr. Issues Mol. Biol. 2024, 46(5), 3990-4003; https://doi.org/10.3390/cimb46050246 - 26 Apr 2024

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Abstract

Retinoic acid (RA) regulates stemness and differentiation in human embryonic stem cells (ESCs). Ewing sarcoma (ES) is a pediatric tumor that may arise from the abnormal development of ESCs. Here we show that RA impairs the viability of SK-ES-1 ES cells and affects the cell cycle. Cells treated with RA showed increased levels of p21 and its encoding gene, CDKN1A. RA reduced mRNA and protein levels of SRY-box transcription factor 2 (SOX2) as well as mRNA levels of beta III Tubulin (TUBB3), whereas the levels of CD99 increased. Exposure to RA reduced the capability of SK-ES-1 to form tumorspheres with high expression of SOX2 and Nestin. Gene expression of CD99 and CDKN1A was reduced in ES tumors compared to non-tumoral tissue, whereas transcript levels of SOX2 were significantly higher in tumors. For NES and TUBB3, differences between tumors and control tissue did not reach statistical significance. Low expression of CD99 and NES, and high expression of SOX2, were significantly associated with a poorer patient prognosis indicated by shorter overall survival (OS). Our results indicate that RA may display rather complex modulatory effects on multiple target genes associated with the maintenance of stem cell’s features versus their differentiation, cell cycle regulation, and patient prognosis in ES. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance)

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