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Drug Resistance Mechanisms in Human Cancer Cells to Anticancer Drugs
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Drug Resistance Mechanisms in Human Cancer Cells to Anticancer Drugs

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

Deadline for manuscript submissions: closed (20 September 2025) | Viewed by 2338

Special Issue Editor

Dr. Daekyu Sun

E-Mail Website
Guest Editor
1. Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ 85721, USA
2. Bio5 Institute, University of Arizona, Tucson, AZ 85721, USA
Interests: DNA chemistry; drug-DNA interaction; G-quadruplex-interactive drugs; anticancer drug discovery; mechanism of actions of new anticancer drugs; transcription factors; DNA repair

Special Issue Information

Dear Colleagues,

The development of resistance to anticancer agents within human cancer cells remains an important area of scientific and clinical investigation. Cancer cells acquire resistance through various mechanisms. New capabilities for repairing DNA damage can arise in response to cytotoxic therapies. Targeted therapies may lose their efficacy due to mutations in the target proteins or epigenetic changes in the expression levels. Cancer cells may even develop mechanisms to inactivate drugs directly. Additionally, resistance arises over time as a result of new mutations. Even as some cells within a tumour remain susceptible to a given treatment, other cells may develop resistance and persist. As a result, a therapeutic strategy that is of interest in new cancer drug development is the use of small molecule inhibitors to target drug resistance mechanisms. This Special Issue, “Drug Resistance Mechanisms in Human Cancer Cells to Anticancer Drugs”, welcomes original research and review articles in the field with a focus on, but not limited to, the molecular and mechanistic basis for drug resistance mechanisms in human cancer cells, as well as new therapeutic strategies for countering these resistance mechanisms.

Dr. Daekyu Sun
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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

  • cancer therapy
  • targeted therapy
  • combination therapy
  • drug resistance
  • resensitization
  • DNA repair
  • DNA damage response
  • DNA repair inhibitors
  • synthetic lethality
  • chemoradiation

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Published Papers (2 papers)

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Research

18 pages, 1362 KB  
Article
The Responsiveness of Breast Cancer Cells to Varied Levels of Vitamin B12, Cisplatin, and G-CSF
by Volkan Aslan, Duygu Deniz Usta, Atiye Seda Yar Sağlam, Ahmet Özet, Osman Sütcüoglu, Kürşat Dikmen and Nuriye Özdemir
Int. J. Mol. Sci. 2025, 26(18), 9086; https://doi.org/10.3390/ijms26189086 - 18 Sep 2025
Viewed by 856
Abstract
Supportive agents, such as vitamin B12 (cobalamin, B12) and granulocyte colony-stimulating factor (G-CSF), are widely used during chemotherapy; however, their direct effects on tumor biology are not well understood. We evaluated the impact of pharmacological B12 and G-CSF, alone or in combination with [...] Read more.
Supportive agents, such as vitamin B12 (cobalamin, B12) and granulocyte colony-stimulating factor (G-CSF), are widely used during chemotherapy; however, their direct effects on tumor biology are not well understood. We evaluated the impact of pharmacological B12 and G-CSF, alone or in combination with cisplatin, on hormone receptor-positive (MCF-7) and triple-negative (MDA-MB-231) breast cancer cells, conducting in vitro assays of cell viability, cytotoxicity, caspase activation, mitochondrial membrane potential, and cytolytic protein expression. Neither B12 nor G-CSF alone induced cytotoxicity; instead, both promoted proliferation in a dose- and time-dependent manner. When combined with cisplatin, they consistently attenuated drug-induced cytotoxicity, suppressed caspase-3/-8/-9 activation, preserved mitochondrial integrity, and reduced perforin/granzyme expression, exhibiting stronger effects in MCF-7 cells. G-CSF markedly increased proliferation (>130% at 50 ng/mL), while B12 modestly enhanced viability and mitigated cisplatin-induced damage, particularly in triple-negative cells. These findings indicate that B12 and G-CSF can impair cisplatin efficacy by blunting apoptotic signaling and mitochondrial injury in different breast cancer subtypes. These preclinical findings warrant prospective, biomarker-driven in vivo and clinical studies to delineate the clinical contexts in which B12 and G-CSF can be safely integrated into supportive care without compromising antitumor efficacy. Full article
(This article belongs to the Special Issue Drug Resistance Mechanisms in Human Cancer Cells to Anticancer Drugs)
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16 pages, 2106 KB  
Article
ERα36 Promotes MDR1-Mediated Adriamycin Resistance via Non-Genomic Signaling in Triple-Negative Breast Cancer
by Muslimbek Mukhammad Ugli Poyonov, Anh Thi Ngoc Bui, Seung-Yeon Lee, Gi-Ho Lee and Hye-Gwang Jeong
Int. J. Mol. Sci. 2025, 26(15), 7200; https://doi.org/10.3390/ijms26157200 - 25 Jul 2025
Viewed by 946
Abstract
Drug resistance remains a critical barrier to effective treatment in several cancers, particularly triple-negative breast cancer (TNBC). Estrogen receptor α36 (ERα36), a variant of the estrogen receptor in ER-negative breast cancer cells, plays important roles in cancer cell proliferation. We investigated the role [...] Read more.
Drug resistance remains a critical barrier to effective treatment in several cancers, particularly triple-negative breast cancer (TNBC). Estrogen receptor α36 (ERα36), a variant of the estrogen receptor in ER-negative breast cancer cells, plays important roles in cancer cell proliferation. We investigated the role of ERα36 in regulating multidrug resistance protein 1 (MDR1) in MDA-MB-231 human breast cancer cells. The activation of ERα36 by BSA-conjugated estradiol (BSA-E2) increased cell viability under Adriamycin exposure, suggesting its involvement in promoting drug resistance. BSA-E2 treatment significantly reduced the intracellular rhodamine-123 levels by activating the MDR1 efflux function, which was linked to increased MDR1 transcription and protein expression. The mechanical ERα36-mediated BSA-E2-induced activation of EGFR and downstream signaling via c-Src led to an activation of the Akt/ERK pathways and transcription factors, NF-κB and CREB. Additionally, ERα36 is involved in activating Wnt/β-catenin pathways to induce MDR1 expression. The silencing of ERα36 inhibited the BSA-E2-induced phosphorylation of Akt and ERK, thereby reducing MDR1 expression via downregulation of NF-κB and CREB as well as Wnt/β-catenin signaling. These findings demonstrated that ERα36 promotes MDR1 expression through multiple non-genomic signaling cascades, including Akt/ERK-NF-κB/CREB and Wnt/β-catenin pathways, and highlight the role of ERα36 as a promising target to enhance chemotherapeutic efficacy in TNBC. Full article
(This article belongs to the Special Issue Drug Resistance Mechanisms in Human Cancer Cells to Anticancer Drugs)
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