Advances in Cancer Biology and Experimental Anticancer Therapies (3rd Edition)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 1008

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Department of Medical and Surgical Sciences -DIMEC, Alma Mater Studiorum, University of Bologna, Via San Giacomo 14, 40126 Bologna, Italy
Interests: immunotoxin; immunoconjugate; immunotargeting; plant toxins; ribosome-inactivating proteins
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Department of Cell Biology and Immunology, Centre of Postgraduate Medical Education, Marymoncka 99/103, 01-813 Warsaw, Poland
Interests: cancer cell biology; biomarkers; micro-RNAs; multidrug resistance; experimental anticancer therapies
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Special Issue Information

Dear Colleagues,

Currently, chemotherapy, surgery, and radiotherapy are the most commonly available cancer treatments. However, despite their demonstrated anti-tumour efficacy, the use of radiotherapy and chemotherapeutic agents has shown many limitations, such as the lack of selectivity for tumour cells, the development of drug resistance, and the appearance of secondary malignancies. As a result, the study and development of alternative targeted therapies, such as immunotherapy and nanotherapy, have been extensively researched in order to find therapies with greater specificity for transformed cells and a lower non-specific toxicity. Therefore, it is essential that we intensify our studies on the molecular mechanisms of carcinogenesis and develop new tactics to diagnose and fight tumours.

In this Special Issue, we aim to provide an update on the most promising anticancer therapeutic strategies and current studies on the molecular factors that influence cancer biology.

Dr. Letizia Polito
Dr. Ewa Gajda
Guest Editors

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Keywords

  • cancer biology
  • experimental anticancer therapies
  • immunotherapy
  • immunotoxins
  • signalling pathways
  • targeted therapies

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Research

16 pages, 5690 KB  
Article
Rhapontigenin Suppresses Leptin-Induced Vasculogenic Mimicry by Inhibiting STAT3-Aquaporin-1 Axis in TNBC Cells
by Seung-Il Wang, Seung-Hyeon Lee and Eun-Ok Lee
Biomedicines 2025, 13(12), 3000; https://doi.org/10.3390/biomedicines13123000 - 7 Dec 2025
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Abstract
Background/Objectives: Vasculogenic mimicry (VM) is a process in which tumor cells form channel structures that resemble blood vessels in shape and function and is increasingly being recognized as a mechanism that contributes to triple-negative breast cancer (TNBC) progression and treatment resistance. Leptin, an [...] Read more.
Background/Objectives: Vasculogenic mimicry (VM) is a process in which tumor cells form channel structures that resemble blood vessels in shape and function and is increasingly being recognized as a mechanism that contributes to triple-negative breast cancer (TNBC) progression and treatment resistance. Leptin, an adipokine that is elevated in patients with obesity, influences VM in breast cancer. Aquaporin-1 (AQP1), a water and solute channel, mediates leptin-induced VM. Rhapontigenin (Rha) is a stilbene derivative that exhibits diverse biological effects, including antioxidant, anti-inflammatory, and anticancer properties. This study investigated whether Rha inhibits leptin-induced VM and whether the mechanism involves AQP1 in TNBC cells. Methods: Cell viability was measured via MTT assay. mRNA and protein expression levels were measured by RT-qPCR and Western blot analysis, respectively. The DNA-binding activity of the signal transducer and activator of transcription 3 (STAT3) was determined using chromatin immunoprecipitation. Invasion and VM tube formation assays were performed. Results: Rha downregulated leptin-induced AQP1 mRNA and protein expression in TNBC cells without cytotoxicity. Phosphorylation of STAT3 by leptin was decreased after Rha treatment. Rha attenuated leptin-induced STAT3 DNA-binding activity at the AQP1 promoter. In addition, Rha inhibited leptin-induced invasion and VM. Consistent with these effects, the expression levels of invasion- and VM-related proteins and matrix metalloproteinase-2 activity were increased by leptin, which was reduced after Rha treatment. Conclusions: These results indicate that Rha inhibits invasive behavior and VM in TNBC cells by interfering with the leptin–STAT3–AQP1 signaling pathway, suggesting that Rha is a promising therapeutic candidate for the treatment of obesity-associated TNBC. Full article
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