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Cancers
Special Issues
State-of-the-Art Mechanisms of Drug Resistance to Targeted Therapy in Cancers
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State-of-the-Art Mechanisms of Drug Resistance to Targeted Therapy in Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: closed (25 November 2024) | Viewed by 4003

Special Issue Editors

Dr. Yan Li

E-Mail Website
Guest Editor
The Centre for Biomedical and Chemical Sciences, School of Science, Faculty of Health and Environmental Sciences, Auckland University of Technology, Auckland 1010, New Zealand
Interests: drug resistance; ABC transporters; natural products; nanomaterials; tyrosine kinase inhibitors
Dr. Johnson Liu

E-Mail Website
Guest Editor
Department of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia
Interests: cancer pharmacology; targeted cancer therapy; pharmacokinetics; drug transport; caner risk related genetic polymorphisms

Special Issue Information

Dear Colleagues,

Drug resistance is an overwhelming challenge in cancer treatment, particularly in the context of targeted therapies. Targeted therapies are designed to inhibit specific proteins or pathways that are critical for tumour growth and progression. While these therapies have been extensively adopted as the standard and preferred regimens, the development of drug resistance often limits their long-term effectiveness. Genetic alterations, bypass signalling, altered drug transport/metabolism, epigenetic changes, tumour heterogeneity, the tumour microenvironment, and adaptive evolution all contribute to tumour resistance.

It is crucial to note that these mechanisms can vary across different cancer types and even among individual patients. Additionally, cancer cells can employ multiple mechanisms simultaneously or develop new resistance mechanisms over time, further complicating treatment strategies. Overcoming drug resistance remains a significant area of research, and ongoing efforts are focused on identifying and targeting these mechanisms in order to develop novel therapeutic strategies and enhance cancer treatment outcomes.

This Special Issue will address subjects related to recent progress on mechanisms of drug resistance to targeted therapy in cancer therapy. It will offer a comprehensive understanding of current progress in the field and highlight perspectives and challenges for the future.

Dr. Yan Li
Dr. Johnson Liu
Guest Editors

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 communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • multidrug resistance (MDR)
  • targeted therapies
  • ABC transporters
  • biomarkers
  • cancer stem-like cells
 

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Published Papers (2 papers)

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Research

14 pages, 3082 KiB  
Article
Interfering Nuclear Protein Laminb1 Induces DNA Damage and Reduces Vemurafenib Resistance in Melanoma Cells In Vitro
by Yuan Li, Yuqing Feng and Dan Chen
Cancers 2024, 16(23), 4060; https://doi.org/10.3390/cancers16234060 - 4 Dec 2024
Cited by 2 | Viewed by 974
Abstract
Background/Objectives: Drug resistance poses a substantial clinical challenge in melanoma treatment, yet the underlying mechanism remains elusive. Here, we report the novel role of laminB1, a nuclear structure protein, in regulating the response of BRAF-mutated melanoma cells to vemurafenib. Results: Our analysis of [...] Read more.
Background/Objectives: Drug resistance poses a substantial clinical challenge in melanoma treatment, yet the underlying mechanism remains elusive. Here, we report the novel role of laminB1, a nuclear structure protein, in regulating the response of BRAF-mutated melanoma cells to vemurafenib. Results: Our analysis of clinical samples and existing databases highlights the tight correlation between the laminB1 expression level and melanoma progression and prognosis. Notably, we observe that laminB1 expression is upregulated when BRAF-mutated melanoma cells develop resistance to vemurafenib. The knockdown of laminB1 substantially increases the sensitivity of melanoma cells to vemurafenib. Furthermore, we found laminB1 suppression increases cell apoptosis via the escalation of DNA damage in a vemurafenib-dose-dependent manner. Conversely, protective cell autophagy is negatively regulated by laminB1 suppression. Interestingly, this distinct regulation pattern of apoptosis and autophagy by laminB1 cooperatively promotes the response of BRAF-mutated melanoma cells to vemurafenib. Conclusions: Our findings unveil the potential of laminB1 as both a diagnosis marker and a therapeutic target of melanoma. Full article
(This article belongs to the Special Issue State-of-the-Art Mechanisms of Drug Resistance to Targeted Therapy in Cancers)
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17 pages, 3956 KiB  
Article
Sperm-Associated Antigen 5 Knockout Reduces Doxorubicin and Docetaxel Resistance in Triple-Negative Breast Cancer MDA-MB-231 and BT549 Cells
by Ji He, Jiawei Li, Yanbiao Liu and Yan Li
Cancers 2024, 16(7), 1269; https://doi.org/10.3390/cancers16071269 - 24 Mar 2024
Viewed by 2291
Abstract
Sperm-associated antigen 5 (SPAG5), also known as Astrin, was previously demonstrated as a biomarker for cellular resistance to major breast cancer therapies, including chemo-, endocrine- and targeted therapy. However, the contribution of SPAG5 to anthracycline- and taxane-based chemotherapy in triple-negative breast cancer (TNBC) [...] Read more.
Sperm-associated antigen 5 (SPAG5), also known as Astrin, was previously demonstrated as a biomarker for cellular resistance to major breast cancer therapies, including chemo-, endocrine- and targeted therapy. However, the contribution of SPAG5 to anthracycline- and taxane-based chemotherapy in triple-negative breast cancer (TNBC) remains controversial. In the present study, the SPAG5 knockout cell model was established by using clustered regularly interspaced palindromic repeats (CRISPR)-CRISPR-associated protein 9 (Cas9) system in MDA-MB-231 and BT549 TNBC cell lines. The knockout of SPAG5 was confirmed on both gene and protein levels using genomic PCR, DNA sequencing and western blotting. The functional loss of SPAG5 was determined by colony-formation assay. SPAG5-regulated doxorubicin- and docetaxel-resistance was assessed by MTT and apoptosis assays. The results indicated that all the SPAG5 knockout MDA-MB-231 and BT549 clones were biallelic, where one allele was replaced by the donor template, and the other allele had the same “T” insertion (indel) adjacent to the cutting sites of gRNAs at the exon 1 boundary, irrespective of the gRNAs and cell lines. The locus of indel interrupted the SPAG5 transcription by damaging the GT-AG mRNA processing rule. Deletion of SPAG5 decreased clonogenicity in both MDA-MB-231 and BT549 cells. SPAG5 was able to regulate the resistance and the drug-induced apoptosis of both doxorubicin and docetaxel. In conclusion, recombinant plasmid-based CRISPR-Cas9 technology can be used to delete the SPAG5 gene in the TNBC cell lines. SPAG5 has an important role in regulating cell proliferation and doxorubicin- and docetaxel-resistance in MDA-MB-231 and BT549 cells. Full article
(This article belongs to the Special Issue State-of-the-Art Mechanisms of Drug Resistance to Targeted Therapy in Cancers)
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