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Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition

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A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (31 December 2025) | Viewed by 40410

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Dr. Peter C. Hart

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College of Pharmacy, Roosevelt University, 1400 N Roosevelt Blvd, Schaumburg, IL 60173, USA
Interests: tumor microenvironment; cell–cell signaling; cell metabolism; hypoxia; oxidative stress; drug repurposing; ovarian cancer; breast cancer
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Dear Colleagues,

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

This Special Issue of Current Issues in Molecular Biology is open for the submission of both original research articles and review articles focused on the advances in our understanding of actionable pharmacologic mechanisms for preventing 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

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Published Papers (10 papers)

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Research

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10 pages, 1947 KB

Open AccessArticle

Evaluation of mTOR, NFκB, and BCL-2 Inhibitor Activity In Vitro on Diffuse Large B-Cell Lymphoma Cells

by Agata Majchrzak, Sylwia Mańka, Barbara Cebula-Obrzut, Aleksandra Mędra, Paweł Robak, Damian Mikulski and Magdalena Witkowska

Curr. Issues Mol. Biol. 2026, 48(2), 229; https://doi.org/10.3390/cimb48020229 - 20 Feb 2026

Cited by 1 | Viewed by 820

Abstract

DLBCLs constitute an aggressive type of lymphoma with varied clinical, molecular and genetic features. The cells are characterized by NFkB pathway disturbances and BCL-2 and mTOR protein deregulation, which significantly inhibit apoptosis. Hence, many treatment strategies have been established to target the functioning of these pathways. While early clinical trials have found mTOR, NFkB and Bcl-2 inhibitors to have activity in many hematological cancers, their activity as monotherapy agents may still be insufficient; therefore, combinations of these compounds with other molecules demonstrating activity in a given cancer subtype are under evaluation. In vitro studies were conducted on the Riva (ABC subtype) and Toledo (GCB subtype) cell lines. Three novel drugs were administered: AZD2014 (vistusertib)—an inhibitor of the serine–threonine kinase mTOR; IMD-0354—an NFκB inhibitor; and ABT-199 (venetoclax)—a highly selective inhibitor for BCL-2. Drugs were administered alone, in pairs and as a combination of all three agents. For the Riva cell line, ABT-199 had the strongest pro-apoptotic effect on cancer cells as monotherapy. As pairs, AZD2014+ABT-199 and ABT-199+IMD0354 demonstrated similar effects. The combination of the three drugs did not have a stronger effect than the drug pairs. For the Toledo cell line, no significant differences were noted between the drugs when used as monotherapy. In pairs, the strongest effect was observed for AZD2014+ABT-199; furthermore, this effect was not intensified by the combination of the three drugs. Our findings, including those for the BCL-2 and mTOR inhibitors, indicate that there is a need for further in vivo studies to evaluate these drugs as potentially effective treatments for DLBCL of the ABC and GCB subtypes. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition)

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20 pages, 13476 KB

Open AccessArticle

Role of UGP2 as a Biomarker in Colorectal Cancer: Implications for Tumor Progression, Diagnosis, and Prognosis

by Lijiao Cui, Caiyuan Yu, Shicai Ye, Yuee Yang, Zhiwei Gu, Vincent Kam Wai Wong and Yu Zhou

Curr. Issues Mol. Biol. 2025, 47(12), 1043; https://doi.org/10.3390/cimb47121043 - 15 Dec 2025

Cited by 1 | Viewed by 839

Abstract

Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide, underscoring the urgent need for reliable biomarkers and therapeutic targets. To address this need, we focused on UDP-glucose pyrophosphorylase 2 (UGP2). Although UGP2 has been implicated in tumorigenesis across multiple cancers, its precise role and clinical significance in CRC remain poorly understood. This study aimed to comprehensively characterize UGP2 in CRC through an integrated approach encompassing proteomic screening, bioinformatics analysis, and experimental validation. We identified UGP2 as a significantly downregulated tumor-suppressive factor in CRC. Specifically, UGP2 expression was significantly downregulated in CRC tissues compared with that in normal controls and exhibited strong correlations with aggressive clinicopathological features, including lymphatic invasion, perineural invasion, and colon polyp history, and patient age. It also demonstrated high diagnostic accuracy in CRC, with an area under the receiver operating characteristic curve (AUC) of 0.990. Reduced UGP2 levels were associated with poorer overall survival and disease-specific survival. Hypermethylation of the UGP2 promoter correlated with a favorable prognosis in patients with CRC. UGP2 expression positively correlated with immune cell infiltration within the tumor microenvironment. Functionally, UGP2 knockdown increased CRC cell proliferation and migration while suppressing apoptosis. Conversely, its overexpression yielded the opposite effects, confirming UGP2’s role in constraining malignant phenotypes. Collectively, these findings establish UGP2 as a key CRC tumor suppressor whose downregulation drives malignant progression and predicts adverse clinical outcomes, suggesting its potential as a dual-purpose diagnostic and prognostic biomarker. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition)

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21 pages, 7221 KB

Open AccessArticle

ADGRG6 Promotes Pancreatic Adenocarcinoma Progression Through the NF-κB/STAT6 Axis and Modulation of the Tumor Immune Microenvironment

by Lisha Li, Zhen Yu, Xuehua Lu, Pei Yang, Shuxia Zhang, Qinghua Lin and Junyong Han

Curr. Issues Mol. Biol. 2025, 47(12), 991; https://doi.org/10.3390/cimb47120991 - 27 Nov 2025

Viewed by 954

Abstract

Background: Adhesion G protein-coupled receptor G6 (ADGRG6), also known as GPR126, has been implicated in several malignancies. However, its expression pattern, clinical significance, and mechanistic role in pancreatic adenocarcinoma (PAAD) remain unclear. Methods: We combined multi-omics analyses, tissue microarray immunohistochemistry, and a series of functional experiments, including 2D and 3D spheroid cultures, zebrafish xenografts, and murine tumor models—to investigate the expression, clinical significance, and mechanism of ADGRG6 in PAAD. The association between ADGRG6 expression and immune infiltration was assessed using TIMER and GEPIA databases, followed by mechanistic validation through ADGRG6 modulation in PAAD cell lines. Results: ADGRG6 was significantly overexpressed in PAAD and correlated with larger tumor size, higher grade, advanced TNM stage, and poor overall survival. Multivariate logistic regression confirmed that high ADGRG6 expression was independently associated with higher pathological grade. Functionally, ADGRG6 silencing markedly inhibited PAAD cell proliferation, migration, and invasion in both 2D and 3D cultures, as well as in zebrafish and nude mouse xenograft models. Integrated transcriptomic and immune analyses revealed that ADGRG6 expression positively correlated with mast cells, macrophages (M1/M2), Th2/Th17 subsets, and interferon–responsive neutrophils. Mechanistically, ADGRG6 silencing reduced STAT6 phosphorylation and GATA3 expression, consistent with the suppression of the NF-κB→STAT6→GATA3 axis. Conclusions: ADGRG6 functions as an oncogenic driver in PAAD, promoting tumor progression and fostering an immunosuppressive microenvironment via NF-κB/STAT6 signaling. These findings not only broaden the mechanistic understanding of ADGRG6 function but also suggest it as a promising target for therapeutic intervention in PAAD. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition)

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15 pages, 3668 KB

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USP30-AS1 Dictates Breast Cancer Cell Fate and Chemoresistance via a miR-3646/FZD7/Wnt/β-Catenin Circuit

by Qian He, Shiyue Yang, Qilei Xin, Yapei Jiang, Li Jiang and Naihan Xu

Curr. Issues Mol. Biol. 2025, 47(12), 974; https://doi.org/10.3390/cimb47120974 - 24 Nov 2025

Cited by 1 | Viewed by 863

Abstract

Cancer stem cells (CSCs) play a pivotal role in promoting tumorigenesis, drug resistance, invasion, and metastasis. Recent studies indicate that long non-coding RNAs (LncRNAs) directly or indirectly regulate CSCs, influencing tumor progression. This study investigated the role of LncRNA USP30-AS1 in maintaining stemness and chemoresistance in breast cancer. USP30-AS1 was significantly upregulated in BCSC-enriched mammospheres derived from MDA-MB-231 and MCF-7 cell lines, where it correlated with elevated stemness markers (CD44, ALDH1A1, OCT4) and an increased proportion of ALDH+ cells. Functional experiments demonstrated that knockdown of USP30-AS1 reduced spheroid formation, stemness marker expression, chemoresistance, migration, and invasion, while its overexpression promoted these phenotypes. Mechanistically, USP30-AS1 acts as a competing endogenous RNA (ceRNA) by sponging miR-3646, which leads to the derepression of Frizzled-7 (FZD7) and subsequent activation of the Wnt/β-catenin signaling pathway. These findings identify USP30-AS1 as a critical promoter of stemness, chemoresistance, and metastasis in BCSCs via the miR-3646/FZD7/Wnt axis, suggesting it is a potential therapeutic target for breast cancer intervention. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition)

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18 pages, 5811 KB

Open AccessArticle

Investigating the Effects of ONC206 Alone and in Combination with Cisplatin on Ovarian Cancer Cell Models

by Sara Mikhael, Rona Fayyad, Leen Abi Harfouch, Varun Vijay Prabhu, Hisham F. Bahmad, Wassim Abou-Kheir and Georges Daoud

Curr. Issues Mol. Biol. 2025, 47(6), 451; https://doi.org/10.3390/cimb47060451 - 12 Jun 2025

Cited by 3 | Viewed by 2326

Abstract

Ovarian cancer (OC) is the most lethal gynecologic malignancy worldwide, with high rates of disease relapse posing a significant therapeutic challenge. Consequently, there is an urgent need to develop novel treatments for OC. This study aims to evaluate the effects of the novel imipridone, ONC206, both as a monotherapy and in combination with the standard of care chemotherapy drug, cisplatin (CDDP), on human OC cell lines. In order to study the effect of ONC206 and CDDP on ovarian cancer, two cell lines, OVCAR-420 and SKOV-3, were used in this study. Cell proliferation was assessed using MTT assay while cell viability was evaluated using the trypan blue exclusion assay. Cell migration was examined using the wound healing assay. To investigate the effects of both treatments, alone or in combination on the stem-cell-like population of OC cells, the sphere-forming assay was employed. Our results revealed that ONC206, alone or in combination with CDDP, exerts a potent anti-proliferative effect on both OVCAR-420 and SKOV-3 cells, as shown in the MTT and trypan blue exclusion assays. Interestingly, a synergistic effect was observed when ONC206 was combined with CDDP, enhancing the overall anti-cancer efficacy. Additionally, ONC206 alone or in combination with CDDP inhibited the migratory ability of the ovarian cancer cells. Furthermore, the activity of ovarian cancer stem cells was inhibited when cells were treated with ONC206 alone or in combination with CDDP, as shown in the significant decrease in both the size and the sphere-forming ability of ovarian cancer stem cells in the 3D culture model. Our results highly suggest the potential of imipridones as a new class of therapeutics in ovarian cancer management. Among these, ONC206 shows nanomolar potency, highlighting its potential as a standalone therapy or in combination with existing treatment regimens. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition)

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16 pages, 11687 KB

Open AccessArticle

Synergistic Antitumor Effects of Ivermectin and Metformin in Canine Breast Cancer via PI3K/AKT/mTOR Pathway Inhibition

by Huili Feng, Lixin He, Talha Umar, Xiao Wang, Wenxuan Li, Bohan Zhang, Xinying Zhu, Ganzhen Deng and Changwei Qiu

Curr. Issues Mol. Biol. 2025, 47(6), 403; https://doi.org/10.3390/cimb47060403 - 29 May 2025

Cited by 2 | Viewed by 19794

Abstract

Ivermectin (IVM) is a macrolide antiparasitic drug, and Metformin (MET) is a biguanide oral hypoglycemic drug. Studies have shown that both of them have obvious anti-tumor effects, but there have been no reports on the combined treatment of Canine breast tumors. This report aimed to investigate the effectiveness and the possible mechanism of drug combination on Canine breast cancers. Mouse breast tumor cells (4T1) and canine breast tumor cells (CMT-1211) were, respectively, treated with IVM, MET, and their combination, and then cell viability was assessed. After that, transcriptomic analysis was performed to study the action pathway of the drug combination with regard to its anti-tumor effects. Reactive oxygen species (ROS) levels were detected by flow cytometry, and autophagosome formation was observed by transmission electron microscopy (TEM). Immunofluorescence detected the cytoplasmic translocation of LC3B and P62 into the nucleus. Western blot detected the protein expressions of LC3B, P62, Beclin1, Bcl-2, p-PI3K, p-AKT, and p-mTOR. Our transcriptomic analysis showed that the combination of IVM and MET regulated the expression of autophagy-related genes and pathways, including the PI3K/AKT/mTOR signaling pathway. Our in vitro experiments showed that the combination of two drugs had a considerably significant effect on cytotoxicity, ROS levels, and the formation of autophagosomes compared to each drug alone. Meanwhile, the in vivo experiments showed that IVM combined with MET had an obvious inhibitory effect on tumor growth in canine breast tumor xenografts. This study concluded that IVM with MET activated autophagy, which killed breast cancer cells by inhibiting the activation of the PI3K/AKT/mTOR pathway and promoting the excessive accumulation of ROS. It offers a theoretical foundation for the synergistic effects of MET and IVM to suppress breast cancer cell activity. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition)

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Review

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26 pages, 2205 KB

Open AccessReview

Evaluating the CRP Interactome: Insights into Possible Novel Roles in Cellular Signaling and Tumorigenicity

by Alison Gerhardt, Dlen Nanakaliy, Harnish D. Shah, Syed Sarfaraz, Charlotte Madigan, Makenna Downing, Robert P. Elliott, Rafid Dipto, Bella Vrapciu, Joseph W. Noetzel, Jessica Armas, Ayesha Ahmed, Marc Potempa, Margaret E. Olson, Lawrence A. Potempa and Peter C. Hart

Curr. Issues Mol. Biol. 2025, 47(12), 1003; https://doi.org/10.3390/cimb47121003 - 28 Nov 2025

Viewed by 1063

Abstract

C-reactive protein (CRP) is a well-known acute phase reactant and putative biomarker for advancing and chronically established inflammation. Its biological activity across its multiple isoforms plays various roles in the initiation, potentiation, and resolution of inflammation. Its molecular signaling within the tissue microenvironment regulates cell–cell communication across cell types (e.g., epithelial cells, endothelial cells, fibroblasts, adipocytes, and immune cells) and affects the development of conditions such as cancer that are subject, at least in part, to inflammatory signaling. Considering the dynamic nature of CRP in modulating disease progression, and the growing evidence of the context-dependent direct molecular activity of CRP on regulating intra- and inter-cellular signaling, it is critical to further understand how this integral molecule alters cell signaling pathways. Although the ability of CRP to directly interact with some extracellular matrix proteins involved with inflammation and disease has been reported as early as the mid-1980s, recent advances in unbiased proteomics have revealed a broader interactome of protein–protein interactions (PPIs) involving CRP. The present study evaluates the CRP PPIs identified to date and explores the potential novel regulatory capacity of CRP on multiple key cellular functions in metabolism and cell–cell signaling, offering an updated framework of the possible biological activities of CRP relevant to tumorigenic processes. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition)

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17 pages, 1448 KB

Open AccessReview

ALK-Targeted Therapy: Resistance Mechanisms and Emerging Precision Strategies

by Ya-Kun Zhang, Jian-Bo Tong, Mu-Xuan Luo, Zhi-Peng Qin and Rong Wang

Curr. Issues Mol. Biol. 2025, 47(12), 996; https://doi.org/10.3390/cimb47120996 - 27 Nov 2025

Cited by 5 | Viewed by 3289

Abstract

Anaplastic lymphoma kinase (ALK), a member of the receptor tyrosine kinase family, plays a central oncogenic role in the initiation and progression of diverse malignancies. Aberrant ALK activation generally results from structural alterations or dysregulated expression, leading to persistent activation of downstream signaling pathways that drive tumor cell proliferation, survival, and metastasis. ALK gene abnormalities predominantly encompass fusions, point mutations, and amplifications, with EML4-ALK-positive non–small cell lung cancer representing a canonical example. The advent of ALK-targeted inhibitors has constituted a major therapeutic milestone for ALK-positive tumors. From first-generation Crizotinib to third-generation Lorlatinib, successive agents have been refined for target selectivity, central nervous system penetration, and coverage of resistance-associated mutations, substantially improving patient survival and intracranial disease control. Nonetheless, the emergence of acquired resistance remains an overarching challenge, mediated by secondary kinase domain mutations, activation of bypass signaling pathways, and tumor phenotypic transformation. This review presents an integrative synthesis of ALK-targeted therapeutic developments, elucidates underlying resistance mechanisms, and surveys emerging strategies, providing a comprehensive perspective on current advances and future directions in precision management of ALK-driven malignancies. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition)

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24 pages, 1399 KB

Open AccessReview

Combination of the First-in-Class Imipridone ONC201 and Standard Anticancer Therapies as a Rational Approach for Therapeutic Benefit

by Brahmi Shenoy, Miloni Mandani, Meena Chintamaneni and Sonal M. Manohar

Curr. Issues Mol. Biol. 2025, 47(9), 775; https://doi.org/10.3390/cimb47090775 - 18 Sep 2025

Cited by 2 | Viewed by 3653

Abstract

The development of drugs for cancer treatment faces critical challenges due to the heterogeneity in cancers, metastatic nature of the disease, lack of efficacy, toxicity, and drug resistance. This makes it quite important to understand the complexities of cancer as well as the limitations of druggable targets. ONC201 (also known as dordaviprone/TIC10/Modeyso^TM), a first-in-class member of the imipridone family, has been shown to kill cancer cells selectively. Recently, it has received FDA approval as the first and only treatment for recurrent H3K27M-mutant diffuse midline glioma. The unique pharmacophore, favorable therapeutic index, ability to induce TRAIL and the integrated stress response (ISR), activation of natural killer cells, and ability to diffuse across the blood–brain barrier are the unique characteristics of ONC201. ONC201 has shown effectiveness against various cancers, and this has been evident in many preclinical studies. ONC201 as a single agent, although useful, has some limitations, which could be addressed by using combination strategies. ONC201 has shown synergism with other drugs, leading to greater tumor cell death or reduced tumor growth. Next-generation imipridones, viz. ONC206 and ONC212, are more potent analogs of ONC201 and exhibit similar characteristics. In this review, we discuss the therapeutic potential of ONC201 and its analogs using combination strategies across different cancers. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition)

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28 pages, 2732 KB

Open AccessReview

Molecular Mechanisms of Radiation Resistance in Breast Cancer: A Systematic Review of Radiosensitization Strategies

by Emma Mageau, Ronan Derbowka, Noah Dickinson, Natalie Lefort, A. Thomas Kovala, Douglas R. Boreham, T. C. Tai, Christopher Thome and Sujeenthar Tharmalingam

Curr. Issues Mol. Biol. 2025, 47(8), 589; https://doi.org/10.3390/cimb47080589 - 24 Jul 2025

Cited by 8 | Viewed by 6105

Abstract

Breast cancer remains one of the most prevalent malignancies worldwide, and radiation therapy is a central component of its management. However, intrinsic or acquired resistance to radiation significantly compromises therapeutic efficacy. This systematic review aimed to identify and evaluate molecular mechanisms and interventions that influence radiation sensitivity in breast cancer models. A comprehensive PubMed search was conducted using the terms “breast cancer” and “radiation resistance” for studies published between 2002 and 2024. Seventy-nine eligible studies were included. The most frequently investigated mechanisms included the dysregulation of the PI3K/AKT/mTOR and MAPK signaling pathways, enhanced DNA damage repair via non-homologous end joining (NHEJ), and the overexpression of cancer stem cell markers such as CD44⁺/CD24⁻/low and ALDH1. Several studies highlighted the role of non-coding RNAs, particularly the lncRNA DUXAP8 and microRNAs such as miR-21, miR-144, miR-33a, and miR-634, in modulating radiation response. Components of the tumor microenvironment, including cancer-associated fibroblasts and immune regulators, also contributed to radiation resistance. By synthesizing current evidence, this review provides a consolidated resource to guide future mechanistic studies and therapeutic development. This review highlights promising molecular targets and emerging strategies to enhance radiosensitivity and offers a foundation for translational research aimed at improving outcomes in radiation-refractory breast cancer. Full article

(This article belongs to the Special Issue Advances in Pharmacotherapeutic Strategies to Prevent Tumor Development, Progression and Treatment Resistance, 2nd Edition)

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