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

Deadline for manuscript submissions: 20 December 2025 | Viewed by 17228

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Dr. Emily Capone

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1. Department of Innovative Technologies in Medicine & Dentistry, University “G. D’Annunzio” of Chieti-Pescara, Chieti, Italy
2. Center for Advanced Studies and Technology (CAST), University “G.D’Annunzio” of Chieti-Pescara, Chieti, Italy
Interests: targeted therapy; tumor biology; monoclonal antibody; antibody drug conjugate; extracellular vesicles
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Dear Colleagues,

Cancer is a chronic disease representing about one-sixth of all global deaths, and to combat it, conventional therapeutic methods, including surgery, radiation therapy, and chemotherapy, have been applied in clinical practice. But it has been observed that these strategies do not effectively differentiate between pathological and normal cells, leading to several adverse effects; therefore, in recent decades, cytotoxic chemotherapy has given way to molecular-targeted drugs that are highly specific and have reduced toxicity. Recently, rapid progress in novel therapeutic strategies coupled with tumor-targeted candidates, containing neoantigens, hormonal agents, molecularly targeted agents, and immune checkpoint inhibitors, has offered new horizons for cancer-related molecular target discovery. Meanwhile, more applications in drug delivery systems have improved targeting, thus enhancing specific drug accumulation in tumor tissues.

We are pleased to invite you to contribute to our Special Issue of the International Journal of Molecular Sciences (IJMS), entitled “Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors”, in order to collect recent advances in the field of molecular targeting, also bringing novel ideas to the scientific community.

This Special Issue aims to expanding current knowledge about the following topics:

The newly discovered molecular targets in tumors;
Recent advances in drug design based on molecular targets;
Recent advances in drug delivery strategies;
Molecular-targeted therapeutic strategies.

In this Special Issue, original research articles and reviews are welcome to be submitted. I look forward to receiving your contributions.

Dr. Emily Capone
Guest Editor

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

targeted therapy
tumor
molecular target
drug delivery
drug design

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Published Papers (11 papers)

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Research

15 pages, 1978 KB

Open AccessArticle

Synthesis and In Vitro Anticancer Evaluation of Novel Phosphonium Derivatives of Chrysin

by Mónika Halmai, Dominika Mária Herr, Szabolcs Mayer, Péter Keglevich, Ejlal A. Abdallah, Noémi Bózsity-Faragó, István Zupkó, Andrea Nehr-Majoros, Éva Szőke, Zsuzsanna Helyes and László Hazai

Int. J. Mol. Sci. 2025, 26(22), 11063; https://doi.org/10.3390/ijms262211063 - 15 Nov 2025

Viewed by 609

Abstract

One of the best-known flavonoid chrysin was coupled at position 7 with several trisubstituted phosphine derivatives with a flexible spacer, and their in vitro anticancer activities were investigated on 60 human tumor cell lines (NCI60) and on several gynecological cancer cells. The trisubstituted phosphines contained different substituents on the aromatic ring(s), e.g., methyl and methoxy groups or fluoro atoms. The phosphorus atom was substituted not only with aromatic rings but with cyclohexyl substituents. The ionic phosphonium building block is important because it allows the therapeutic agents to transfer across the cell membrane. Therefore, the pharmacophores linked to it can exert their effects in the mitochondria. Instead of the ionic phosphonium element, a neutral moiety, namely the triphenylmethyl group, was also added to the side chain, being sterically similar but without a charge and phosphorus atom. Most of the hybrids exhibited low micromolar growth inhibition (GI₅₀) values against the majority of the tested cell lines. Notably, conjugate 3f stood out, demonstrating nanomolar antitumor activity against the K-562 leukemia cell line (GI₅₀ = 34 nM). One selected compound (3i) with promising cancer selectivity elicited cell cycle disturbances and inhibited the migration of breast cancer. The tumor-selectivity of 3a and 3f was assessed based on their effects on non-tumor Chinese hamster ovary (CHO) cells using the CellTiter-Glo Luminescent Cell Viability Assay. Given their estimated half-maximal inhibitory concentration (IC₅₀) values on non-tumor CHO cells (2.65 µM and 1.15 µM, respectively), these conjugates demonstrate promising selectivity toward several cancer cell lines. The excellent results obtained may serve as good starting points for further optimization and the design of even more effective flavonoid- and/or phosphonium-based drugs. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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12 pages, 4939 KB

Open AccessArticle

Levobupivacaine Administration Suppressed Cell Metabolism in Human Adenocarcinoma A549 Cells

by Masae Iwasaki, Makiko Yamamoto, Masahiro Tomihari, Kaori Fujii and Masashi Ishikawa

Int. J. Mol. Sci. 2025, 26(22), 10833; https://doi.org/10.3390/ijms262210833 - 7 Nov 2025

Viewed by 327

Abstract

Perioperative anesthesia might directly alter cancer cell biology. We investigated the effects of levobupivacaine treatment on lung adenocarcinoma cells. A549 cells were treated with levobupivacaine at concentrations of 0.1 mM and 0.5 mM for 2 h. Transfection with angiotensin-converting enzyme 2 (ACE2) small interfering RNA (siRNA) was performed 6 h before the levobupivacaine treatment. Cell proliferation was assessed using a cell counting kit 8 (CCK-8), and ATP synthesis was evaluated with the CellTiter-Glo^® 2.0 assay at 0 and 24 h after anesthesia exposure. RT-PCR was performed to examine various biomarkers. The levobupivacaine treatment suppressed ATP synthesis without affecting cell proliferation. This was associated with the upregulation of ACE2 and the downregulation of pro-cancer biomarkers, including HIF-1α, MMP-9, and β-catenin. The anticancer effect of levobupivacaine was negated when ACE2 siRNA was introduced, and it was further suppressed when combined with levobupivacaine. The RT-PCR results indicated that the expressions of B-cell/CLL lymphoma 2 (BCL2) and wingless/integrated 1 (WNT1) were reduced after levobupivacaine treatment, but these effects were reversed with ACE2 siRNA induction. The administration of levobupivacaine suppressed A549 cell metabolism and downregulated HIF-1α, MMP-9, WNT1, EGFR, and BCL2 in an ACE2-dependent manner. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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16 pages, 1863 KB

Open AccessArticle

Validating TDP1 as an Inhibition Target for Lipophilic Nucleoside Derivative in Human Cells

by Irina A. Chernyshova, Tatyana E. Kornienko, Nadezhda S. Dyrkheeva, Alexandra L. Zakharenko, Arina A. Chepanova, Konstantin E. Orishchenko, Nikolay N. Kurochkin, Mikhail S. Drenichev and Olga I. Lavrik

Int. J. Mol. Sci. 2025, 26(20), 10193; https://doi.org/10.3390/ijms262010193 - 20 Oct 2025

Viewed by 572

Abstract

Tyrosyl-DNA phosphodiesterase 1 (TDP1) is an important DNA repair enzyme and its functioning is considered as one of the possible reasons for tumor resistance to topoisomerase 1 (TOP1) poisons such as topotecan. Thus, TDP1 inhibitors in combination with topotecan may improve the effectiveness of anticancer therapy. TDP1 acts somehow in a phospholipase manner, depleting the phosphodiester bond between lipophilic tyrosine residue and 3′ end of DNA; therefore, lipophilic molecules bearing aromatic substituents can interact with TDP1 and even possess high inhibitory activity, which is evidenced by data from the literature. Previously, we identified lipophilic nucleoside derivative (compound 6d, IC₅₀ = 0.82 µM) as an effective inhibitor of the purified enzyme TDP1 that enhances the cytotoxic, DNA-damaging, and antitumor effects of topotecan. However, the role of TDP1 inhibition in this synergistic effect remained not fully understood. In the present study, we have tested the hypothesis of a TDP1-dependent mechanism of action for compound 6d, showing that it sensitizes wild-type A549 lung cancer cells, but not TDP1 knockout cells, to the cytotoxic effects of topotecan. The sensitizing effect was absent in non-cancerous HEK293A cells regardless of TDP1 status. Additionally, we analyzed the effect of compound 6d and topotecan on the expression level of TOP1 and TDP1 to determine whether the observed synergy was due to direct TDP1 inhibition and/or changes in regulation of these enzymes. The data obtained shows that compound 6d did not affect TDP1 gene expression level in HEK293A and A549 WT cells. Thus, compound 6d most probably does not suppress the transcription or mRNA stability of TDP1, and the synergistic action of 6d with topotecan is related to TDP1 inhibtion. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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27 pages, 3604 KB

Open AccessArticle

Predicting Survival in Bevacizumab-Treated Colorectal Cancer: Personalized Mathematical Models Based on Clinical and Angiogenic Biomarkers

by Diana Cornelia Moisuc, Mihai Vasile Marinca, Bogdan Gafton, Daniela Constantinescu, Petru Cianga and Mariana Pavel-Tanasa

Int. J. Mol. Sci. 2025, 26(19), 9332; https://doi.org/10.3390/ijms26199332 - 24 Sep 2025

Viewed by 1207

Abstract

Aberrant activation of proangiogenic signaling pathways, particularly the vascular endothelial growth factor (VEGF) axis, drives neovascularization and tumor progression in colorectal cancer (CRC). Bevacizumab targets VEGF-A-mediated angiogenesis, but the lack of validated predictive biomarkers limits personalized treatment. In this prospective study, we evaluated a panel of circulating angiogenic biomarkers combined with clinical parameters, using mathematical models to predict survival in metastatic CRC patients treated with bevacizumab and chemotherapy. Low VEGF-A and VEGF-D levels, together with high bFGF, were associated with improved overall survival (OS). A logistic regression model incorporating these biomarkers, regional lymph node invasion, and primary tumor resection status showed significant prognostic accuracy (p < 0.001). Incorporating CypA further refined the model, identifying patients with low VEGF-A, VEGF-D, and CypA, and high VEGF-C and PlGF, as having the most favorable OS. These findings demonstrate that integrating clinical and circulating biomarker data can improve individualized risk assessment and support personalized therapeutic strategies for CRC patients receiving bevacizumab. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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17 pages, 6254 KB

Open AccessArticle

Pro-Apoptotic Effects of Unsymmetrical Bisacridines in 3D Pancreatic Multicellular Tumor Spheroids

by Agnieszka Kurdyn, Ewa Paluszkiewicz and Ewa Augustin

Int. J. Mol. Sci. 2025, 26(15), 7557; https://doi.org/10.3390/ijms26157557 - 5 Aug 2025

Cited by 1 | Viewed by 815

Abstract

Pancreatic cancer (PC) is an aggressive malignancy with a poor prognosis, requiring innovative approaches to evaluate new therapies. Considering the high activity of unsymmetrical bisacridines (UAs) in PC monolayer cultures, we employed multicellular tumor spheroids (MCTS) to assess whether UAs retain pro-apoptotic activity under more physiologically relevant conditions. Ultra-low attachment plates were used to form spheroids from three PC cell lines (Panc-1, MIA PaCa-2, and AsPC-1) with different genotypes and phenotypes. The effects of UA derivatives (C-2028, C-2045, and C-2053) were evaluated using microscopy and flow cytometry (7-AAD for viability and annexin V-FITC/PI for membrane integrity). UAs altered the morphology of the spheroids and reduced their growth. Notably, Panc-1 spheroids exhibited compromised integrity. The increase in 7-AAD⁺ cells confirmed diminished cell viability, and annexin V-FITC assays showed apoptosis as the dominant death pathway. Interestingly, the exact derivative was most active against a given cell line regardless of culture conditions. These results confirm that UAs maintain anticancer activity in 3D cultures and induce apoptosis, with varying efficacy across different cell lines. This underscores the value of diverse cellular models in compound evaluation and supports UAs as promising candidates for pancreatic cancer therapy. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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21 pages, 1655 KB

Open AccessArticle

The Design of a Multistage Monitoring Protocol for Dendritic Cell-Derived Exosome (DEX) Immunotherapy: A Conceptual Framework for Molecular Quality Control and Immune Profiling

by Ramón Gutiérrez-Sandoval, Francisco Gutiérrez-Castro, Natalia Muñoz-Godoy, Ider Rivadeneira, Adolay Sobarzo, Luis Alarcón, Wilson Dorado, Andy Lagos, Diego Montenegro, Ignacio Muñoz, Rodrigo Aguilera, Jordan Iturra, Francisco Krakowiak, Cristián Peña-Vargas and Andrés Toledo

Int. J. Mol. Sci. 2025, 26(12), 5444; https://doi.org/10.3390/ijms26125444 - 6 Jun 2025

Cited by 1 | Viewed by 1258

Abstract

The increasing complexity of dendritic cell (DC)-derived exosome (DEX) immunotherapy demands structured monitoring protocols capable of translating molecular activity into actionable clinical outputs. This study proposes a standardized, multistage immunomonitoring framework designed to evaluate immune activation, cytokine polarization, and product integrity in DEX-based therapies. The protocol integrates open access methodologies—flow cytometry, cytometric bead array (CBA), and Western blotting—to assess CD69/CD25 activation, Th1/Th2/Th17 cytokine profiles, and vesicle identity across distinct checkpoints. These outputs are consolidated within the Structured Immunophenotypic Traceability Platform (STIP), which applies logic-based classifications (Type I–III) to support reproducible stratification of immune responses. Functional validation was performed through ex vivo co-culture models, enabling real-time interpretation of immune polarization, cytotoxic potential, and batch consistency. These outputs are supported by previous experimental validations published in Cancers and Biomedicines (2025), where PLPC and DC-derived vesicles demonstrated immunological consistency and a phenotypic stratification capacity. This approach provides a scalable monitoring structure that can support personalized treatment decisions, quality assurance workflows, and integration into regulatory documentation (e.g., CTD Module 5.3) for early-phase, non-pharmacodynamic immunotherapies. This conceptual protocol does not aim to demonstrate therapeutic efficacy but to provide a reproducible documentation framework for real-world immune monitoring and regulatory alignment in vesicle-based immunotherapy. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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16 pages, 498 KB

Open AccessArticle

The Predictive Impact of HPV Genotypes, Tumor Suppressors and Local Immune Response in the Regression of Cervical Intraepithelial Neoplasia 2-3: A Prospective Population-Based Cohort Study

by Pavla Sustova, Birgit Engesæter, Irene Tveiterås Øvestad, Einar G. Gudlaugsson, Reza Ghiasvand, Ivar Skaland, Jan P. A. Baak, Ameli Tropé, Emiel A. M. Janssen and Ane Cecilie Munk

Int. J. Mol. Sci. 2025, 26(11), 5205; https://doi.org/10.3390/ijms26115205 - 28 May 2025

Cited by 1 | Viewed by 3335

Abstract

Cervical intraepithelial neoplasia (CIN) is caused by human papillomavirus (HPV); however, factors such as HPV genotype and individual immune response may also contribute to its development. The loop electrosurgical excision procedure (LEEP) is a treatment for high-grade cervical intraepithelial neoplasia (CIN), as approximately 30% of these cases may progress to cancer. However, 20–40% of cases will regress spontaneously. HPV16 infection constitutes the highest risk for progression to cervical cancer and a lower probability of regression. Knowledge regarding the regression of lesions caused by other high-risk genotypes alone or in association with biomarker expression and lesion length has been limited. In the present study, the regression rates of high-grade squamous intraepithelial lesions were calculated. Twenty-one percent of the 161 women diagnosed with CIN2-3 on colposcopy-directed biopsies exhibited regression (defined as CIN1 or less) in the subsequent cone excisions. The mean interval between biopsy and treatment was 113 days (range of 71–171). High-grade lesions of the squamous epithelium caused by HPV16, together with lesions caused by HPV31, 52 and 58, showed significantly lower regression rates (HR 0.54, 0.22–0.75; low-regression group) than lesions caused by HPV18, 33, 35, 39, and 45 (HR 2.85, 1.54–5.28; high-regression group). A multivariate analysis of HPV genotypes, epithelial expressions of pRb and p53, immune cell proportions in the stroma (CD4/CD25 and CD4/CD8), and lesion lengths correctly predicted regression in 78% (Harrell’s C). A Harrell’s C value of 82% for the low-regression group indicates that different HPV genotypes or groups, together with divergent patterns of tumor suppressors, immune cells, and lesion size, can give prognostic information regarding the outcome of CIN2-3. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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25 pages, 3487 KB

Open AccessArticle

AI-Driven Drug Target Screening Platform Identified Oncogene CACNA2D1 Activated by Enhancer Infestation in Epstein-Barr Virus-Associated Nasopharyngeal Carcinoma

by Dittman Lai-Shun Chung, Geoffrey Ho Duen Leung, Songran Liu, Sarah Wing Yan Lok, Ying Xin, Yunfei Xia, Alex Zhavoronkov, Frank W. Pun, Wai-Tong Ng and Wei Dai

Int. J. Mol. Sci. 2025, 26(10), 4697; https://doi.org/10.3390/ijms26104697 - 14 May 2025

Cited by 1 | Viewed by 1974

Abstract

The management of nasopharyngeal cancer (NPC) is rapidly evolving, with immune checkpoint inhibitors emerging as a prominent treatment approach. However, drug development targeting specific molecular and cellular abnormalities in NPC has slowed. Recent advancements in artificial intelligence (AI) and bioinformatics, particularly those integrating multi-omics data, offer a more effective alternative to traditional in vitro screening methods for identifying clinically actionable targets in NPC. Through a combination of multi-omics analyses and AI-driven screening, we identified CACNA2D1 as a novel cancer-cell-specific therapeutic target in NPC. Our research indicates that exploiting Epstein–Barr virus (EBV) tethering increases H3K27 acetylation near the CACNA2D1 promoter. Analysis of clinical specimens revealed significant upregulation of CACNA2D1 at both the transcriptional and translational levels (p-value < 0.01). Functional studies demonstrated that the mouse tumour size shrank by one-third upon the depletion of CACNA2D1, and there was an 85% reduction in cancer cell growth through the blockage of enhancers, while the presence of CACNA2D1 conferred a survival advantage during NPC tumour development. These findings highlight the potential of CACNA2D1 as a promising target for therapeutic intervention in NPC. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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17 pages, 5546 KB

Open AccessArticle

ANKRD2 Knockdown as a Therapeutic Strategy in Osteosarcoma: Effects on Proliferation and Drug Response in U2OS and HOS Cells

by Vittoria Cenni, Alberto Bavelloni, Cristina Capanni, Elisabetta Mattioli, Federico Bortolozzo, Snezana Kojic, Giulia Orlandi, Jessika Bertacchini and William L. Blalock

Int. J. Mol. Sci. 2025, 26(4), 1736; https://doi.org/10.3390/ijms26041736 - 18 Feb 2025

Viewed by 1710

Abstract

Ankrd2, a mechanoresponsive protein primarily studied in muscle physiology, is emerging as a player in cancer progression. This study investigates the functional role of Ankrd2 in osteosarcoma cells, revealing its critical involvement in cell proliferation and response to chemotherapeutic drugs. We showed that Ankrd2 knockdown impairs the activation of PI3K/Akt and ERK1/2 pathways, reduces levels of cell cycle regulators including cyclin D1 and cyclin B, and counteracts the expression of nuclear lamin A and lamin B, disrupting nuclear morphology and DNA integrity. Strikingly, the loss of Ankrd2 enhances the sensitivity of osteosarcoma cells to doxorubicin and cisplatin, highlighting Ankrd2 potential as a therapeutic target to improve chemotherapeutic efficacy. Defining a novel mechanistic role for Ankrd2 in promoting tumor progression, we propose that Ankrd2 reduction could be exploited as an adjuvant strategy to enhance the efficacy of chemotherapy, offering new therapeutic opportunities for OS treatment. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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16 pages, 4096 KB

Open AccessArticle

Enhancing Radiation Therapy Response in Prostate Cancer Through Metabolic Modulation by Mito-Lonidamine: A ¹H and ³¹P Magnetic Resonance Spectroscopy Study

by Stepan Orlovskiy, Pradeep Kumar Gupta, Fernando Arias-Mendoza, Dinesh Kumar Singh, Skyler Nova, David S. Nelson, Vivek Narayan, Cameron J. Koch, Micael Hardy, Ming You, Balaraman Kalyanaraman and Kavindra Nath

Int. J. Mol. Sci. 2025, 26(2), 509; https://doi.org/10.3390/ijms26020509 - 9 Jan 2025

Viewed by 2055

Abstract

Radiation therapy (RT) is the cornerstone treatment for prostate cancer; however, it frequently induces gastrointestinal and genitourinary toxicities that substantially diminish the patients’ quality of life. While many individuals experience transient side effects, a subset endures persistent, long-term complications. A promising strategy to mitigate these toxicities involves enhancing tumor radiosensitivity, potentially allowing for lower radiation doses. In this context, mito-lonidamine (Mito-LND), an antineoplastic agent targeting the mitochondrial electron transport chain’s complexes I and II, emerges as a potential radiosensitizer. This study investigated Mito-LND’s capacity to augment RT efficacy and reduce adverse effects through comprehensive in vitro and in vivo assessments using hormone-sensitive and hormone-refractory prostate cancer models. Employing a Seahorse analysis and ¹H/³¹P magnetic resonance spectroscopy (MRS), we observed that Mito-LND selectively suppressed lactate production, decreased intracellular pH, and reduced bioenergetics and oxygen consumption levels within tumor cells. These findings suggest that Mito-LND remodels the tumor microenvironment by inducing acidification, metabolic de-energization, and enhanced oxygenation, thereby sensitizing tumors to RT. Our results underscore the potential of Mito-LND as a therapeutic adjunct in RT to improve patient outcomes and reduce radiation-associated toxicities in early-stage prostate cancer. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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17 pages, 14804 KB

Open AccessArticle

A Role for Periostin Pathological Variants and Their Interaction with HSP70-1a in Promoting Pancreatic Cancer Progression and Chemoresistance

by Yasuo Tsunetoshi, Fumihiro Sanada, Yuko Kanemoto, Kana Shibata, Atsushi Masamune, Yoshiaki Taniyama, Koichi Yamamoto and Ryuichi Morishita

Int. J. Mol. Sci. 2024, 25(23), 13205; https://doi.org/10.3390/ijms252313205 - 8 Dec 2024

Cited by 2 | Viewed by 2283

Abstract

Pancreatic ductal adenocarcinoma (PDAC) characterized by an abundant cancer stroma is an aggressive malignancy with a poor prognosis. Periostin (Pn) is a key extracellular matrix (ECM) protein in various tumor progression. Previously, we described the role of Pn alternative splicing variants (ASVs) with specific functional features in breast cancer. Pn is known to associate with a chemoresistance of PDAC, but the functions of the Pn-ASVs remain largely unknown. In this study, we focused on physiological and pathological Pn-ASVs, and examined the characteristics of Pn-expressing cells and the difference in function of each ASV. We found that cancer-associated fibroblasts (CAFs) are a main source of Pn synthesis, which selectively secrete pathological Pn-ASVs with exon 21 both in mouse and human samples. RNA sequencing identified a gene signature of Pn-positive CAFs associated with ECM-related genes and chemokines, factors that shape the chemoresistance tumor microenvironment (TME). Additionally, only pathological Pn-ASVs interacted with heat shock protein 70-1a (HSP70-1a), leading to significant rescue of gemcitabine-induced PDAC apoptosis. In silico analysis revealed that the presence or absence of exon 21 changes the tertiary structure of Pn and the binding sites for HSP70-1a. Altogether, Pn-ASVs with exon 21 secreted from CAFs play a key role in supporting tumor growth by interacting with cancer cell-derived HSP70-1a, indicating that Pn-ASVs with exon 21 might be a potential therapeutic and diagnostic target in PDAC patients with rich stroma. Full article

(This article belongs to the Special Issue Recent Advances in Molecular Targets for Treatment and Drug Delivery in Tumors)

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