Cancer Pharmacology

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Drug Discovery, Development and Delivery".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 547

Special Issue Editor


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Guest Editor
Department of Cell Biology & Institute of Biomedicine, Jinan University, Guangzhou, China
Interests: cancer cell biology; cancer pharmacology; anticancer drug; drug resistance; signal transduction
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Special Issue Information

Dear Colleagues,

Cancer pharmacology is a dynamic and rapidly advancing field, driving the discovery and development of novel therapies to overcome cancer. This Special Issue showcases cutting-edge progress in drug development, molecular targeting, and personalized medicine, providing novel insights into overcoming drug resistance and enhancing therapeutic outcomes. We invite contributions spanning a broad spectrum of topics, including, but not limited to, the following:

  • Mechanisms of anticancer drugs and drug resistance;
  • Targeted therapies and precision medicine;
  • Immunopharmacology and cancer immunotherapy;
  • Innovative drug delivery systems;
  • Pharmacogenomics and biomarker discovery;
  • Combination therapies and synergistic drug interactions;
  • Preclinical and clinical oncology research.

By highlighting these key areas, this Special Issue aims to foster collaboration and accelerate breakthroughs in cancer treatment.

We welcome original research articles, reviews, and short communications that encompass fundamental and applied research in cancer pharmacology. We are particularly interested in studies that employ cutting-edge technologies, such as multi-omics approaches, high-throughput screening, and computational modeling, to advance our understanding of drug mechanisms and optimize therapeutic outcomes.

By bringing together diverse perspectives, this Special Issue seeks to foster innovation and collaboration in the fight against cancer. We invite researchers and clinicians to contribute their latest findings and insights to this important collection.

Prof. Dr. Zhi Shi
Guest Editor

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Keywords

  • cancer pharmacology
  • anticancer drug
  • cancer chemotherapy
  • targeted therapy
  • cancer immunotherapy
  • combination therapy
  • drug resistance

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Published Papers (1 paper)

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Research

14 pages, 5033 KB  
Article
H89 Reverses Multidrug Resistance in Colorectal Cancer by Inhibiting the ATPase Activity of ABCB1
by Wei-Jing Liu, Yi-Yao Shan, Huan Wang, Yu-Meng Xiong, Le-Yao Shi, Xiao-Peng Song, Min Li, Ke He, Jia Huang and Zhi Shi
Biomedicines 2025, 13(12), 2869; https://doi.org/10.3390/biomedicines13122869 - 25 Nov 2025
Viewed by 378
Abstract
Background: Multidrug resistance (MDR) remains a major obstacle in cancer chemotherapy, and overexpression of ABCB1 plays a critical role in the pathogenesis of MDR. Despite decades of research, significant clinical progress in the development of ABCB1 inhibitors has yet to be achieved. The [...] Read more.
Background: Multidrug resistance (MDR) remains a major obstacle in cancer chemotherapy, and overexpression of ABCB1 plays a critical role in the pathogenesis of MDR. Despite decades of research, significant clinical progress in the development of ABCB1 inhibitors has yet to be achieved. The small-molecule H89 is originally identified as an inhibitor of protein kinase A (PKA), but it also exhibits various functions unrelated to the PKA. This study investigates H89 as a novel ABCB1-inhibitor to reverse MDR in colorectal cancer (CRC). Methods: Cytotoxicity assays were performed on ABCB1-overexpressing MDR cell line HCT-8/V and parental CRC cell line HCT-8. Drug accumulation was quantified via flow cytometry, and cell cycle effects were analyzed using propidium iodide staining. The ATPase activity of ABCB1 was detected using an ATPase activity assay kit. Molecular docking utilized the ABCB1 crystal structure. Results: Both 3 μM and 10 μM H89 significantly reverses resistance to two ABCB1 substrate drugs (doxorubicin and vincristine) in HCT-8/V cells in a dose-dependent manner, with no such effect observed inHCT-8 cells. The combination of H89 and doxorubicin or vincristine resulted in a significant increase in the proportion ofHCT-8/Vcells in the sub-G1 and G2/M phases. Further mechanistic studies reveal that H89 exerts its effect by inhibiting the drug efflux function of ABCB1, thereby increasing the intracellular accumulation of the substrate drugs and reversing multidrug resistance. Furthermore, H89 did not alter the expression of ABCB1. H89 effectively inhibited the ATPase activity of ABCB1. Molecular docking simulations revealed the binding mode of H89 with ABCB1. Conclusions: The combination of H89 with ABCB1 substrate drugs significantly reverses multidrug resistance in colorectal cancer. These findings provide a strong theoretical and experimental foundation for the development of novel MDR-reversing agents targeting ABCB1. Full article
(This article belongs to the Special Issue Cancer Pharmacology)
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