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New Insights into Overcoming Drug Resistance in Cancers
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New Insights into Overcoming Drug Resistance in Cancers

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: closed (15 July 2023) | Viewed by 8595

Special Issue Editor

Dr. Fazlul Huq

E-Mail Website
Guest Editor
Retired Academic, School of Medical Sciences, The University of Sydney, Sydney, Australia
Interests: metal based anticancer drugs; tumour active phytochemicals; synergism; combination index; proteomics; artificial intelligence
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chemotherapeutic drugs such as cisplatin, carboplatin and oxaliplatin in spite of toxic side effects and problems of acquired drug resistance are still widely used to treat various cancers. In recent times many other metal based tumour active compounds such as compounds of ruthenium have come to increasing attention although almost all have problems of side effects. Tumour active phytochemicals known to be largely freed from side effects can be ideal candidates for combination with targeted therapy towards overcoming drug resistance and reducing side effects. This special issue will focus on combination of chemotherapeutic drugs with tumour phytochemicals towards overcoming drug resistance and reducing side effects in cancers.

Dr. Fazlul Huq
Guest Editor

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Keywords

  • phytochemicals
  • drug combination
  • combination index
  • ovarian cancer
  • colorectal cancer
  • DNA damage
  • oxidative stress
  • proteomics
  • heat shock proteins

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Published Papers (4 papers)

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Research

15 pages, 10656 KiB  
Article
Targeting Glutaminolysis Shows Efficacy in Both Prednisolone-Sensitive and in Metabolically Rewired Prednisolone-Resistant B-Cell Childhood Acute Lymphoblastic Leukaemia Cells
by Yordan Sbirkov, Bozhidar Vergov, Vasil Dzharov, Tino Schenk, Kevin Petrie and Victoria Sarafian
Int. J. Mol. Sci. 2023, 24(4), 3378; https://doi.org/10.3390/ijms24043378 - 8 Feb 2023
Cited by 3 | Viewed by 1815
Abstract
The prognosis for patients with relapsed childhood acute lymphoblastic leukaemia (cALL) remains poor. The main reason for treatment failure is drug resistance, most commonly to glucocorticoids (GCs). The molecular differences between prednisolone-sensitive and -resistant lymphoblasts are not well-studied, thereby precluding the development of [...] Read more.
The prognosis for patients with relapsed childhood acute lymphoblastic leukaemia (cALL) remains poor. The main reason for treatment failure is drug resistance, most commonly to glucocorticoids (GCs). The molecular differences between prednisolone-sensitive and -resistant lymphoblasts are not well-studied, thereby precluding the development of novel and targeted therapies. Therefore, the aim of this work was to elucidate at least some aspects of the molecular differences between matched pairs of GC-sensitive and -resistant cell lines. To address this, we carried out an integrated transcriptomic and metabolomic analysis, which revealed that lack of response to prednisolone may be underpinned by alterations in oxidative phosphorylation, glycolysis, amino acid, pyruvate and nucleotide biosynthesis, as well as activation of mTORC1 and MYC signalling, which are also known to control cell metabolism. In an attempt to explore the potential therapeutic effect of inhibiting one of the hits from our analysis, we targeted the glutamine-glutamate-α-ketoglutarate axis by three different strategies, all of which impaired mitochondrial respiration and ATP production and induced apoptosis. Thereby, we report that prednisolone resistance may be accompanied by considerable rewiring of transcriptional and biosynthesis programs. Among other druggable targets that were identified in this study, inhibition of glutamine metabolism presents a potential therapeutic approach in GC-sensitive, but more importantly, in GC-resistant cALL cells. Lastly, these findings may be clinically relevant in the context of relapse—in publicly available datasets, we found gene expression patterns suggesting that in vivo drug resistance is characterised by similar metabolic dysregulation to what we found in our in vitro model. Full article
(This article belongs to the Special Issue New Insights into Overcoming Drug Resistance in Cancers)
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23 pages, 8900 KiB  
Article
Analysis of Changes in the Expression of Selected Genes from the ABC Family in Patients with Triple-Negative Breast Cancer
by Anna Makuch-Kocka, Janusz Kocki, Anna Brzozowska, Jacek Bogucki, Przemysław Kołodziej and Anna Bogucka-Kocka
Int. J. Mol. Sci. 2023, 24(2), 1257; https://doi.org/10.3390/ijms24021257 - 9 Jan 2023
Cited by 2 | Viewed by 2175
Abstract
Triple-negative breast cancer (TNBC) is characterized by a lack of expression of hormone receptors (estrogen and progesterone), as cancer cells also do not overexpress the HER2 receptor. Due to their molecular profile, treatments for this type of breast cancer are limited. In some [...] Read more.
Triple-negative breast cancer (TNBC) is characterized by a lack of expression of hormone receptors (estrogen and progesterone), as cancer cells also do not overexpress the HER2 receptor. Due to their molecular profile, treatments for this type of breast cancer are limited. In some cases, the pharmacotherapy of patients with TNBC is hindered by the occurrence of multidrug resistance, which is largely conditioned by proteins encoded by genes from the ABC family. The aim of our study was to determine the expression profile of 14 selected genes from the ABC family using real-time PCR in 68 patients with TNBC by comparing the obtained results with clinical data and additionally using bioinformatics tools (Ualcan and The Breast Cancer Gene Expression Miner v4.8 (bc -GenExMiner v4.8)), as well as by comparing experimental data with data in the Cancer Genome Atlas (TCGA) database. Based on the conducted studies, we found different levels of gene expression depending on the age of patients, tumor sizes, metastases to lymph nodes, cell infiltration into adipose tissue, tumor stages, or lymphovascularinvasion. The results of the presented studies demonstrate the effect of the expression level of the studied genes on the clinical course and prognosis of patients with TNBC, and suggest how profiling the expression level of genes from the ABC family may be a useful tool in determining personalized TNBC treatment. Full article
(This article belongs to the Special Issue New Insights into Overcoming Drug Resistance in Cancers)
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15 pages, 2321 KiB  
Article
PKR-Mediated Phosphorylation of eIF2a and CHK1 Is Associated with Doxorubicin-Mediated Apoptosis in HCC1143 Triple-Negative Breast Cancer Cells
by Sol Lee, Ha-Yeon Jee, Yoon-Gyeong Lee, Jong-Il Shin, Yong-Joon Jeon, Ji-Beom Kim, Hye-eun Seo, Ji-Yeon Lee and Kyungho Lee
Int. J. Mol. Sci. 2022, 23(24), 15872; https://doi.org/10.3390/ijms232415872 - 14 Dec 2022
Cited by 4 | Viewed by 2240
Abstract
Triple-negative breast cancer is more aggressive than other types of breast cancer. Protein kinase R (PKR), which is activated by dsRNA, is known to play a role in doxorubicin-mediated apoptosis; however, its role in DNA damage-mediated apoptosis is not well understood. In this [...] Read more.
Triple-negative breast cancer is more aggressive than other types of breast cancer. Protein kinase R (PKR), which is activated by dsRNA, is known to play a role in doxorubicin-mediated apoptosis; however, its role in DNA damage-mediated apoptosis is not well understood. In this study, we investigated the roles of PKR and its downstream players in doxorubicin-treated HCC1143 triple-negative breast cancer cells. Doxorubicin treatment induces DNA damage and apoptosis. Interestingly, doxorubicin treatment induced the phosphorylation of eukaryotic initiation factor 2 alpha (eIF2α) via PKR, whereas the inhibition of PKR with inhibitor C16 reduced eIF2α phosphorylation. Under these conditions, doxorubicin-mediated DNA fragmentation, cell death, and poly(ADP ribose) polymerase and caspase 7 levels were recovered. In addition, phosphorylation of checkpoint kinase 1 (CHK1), which is known to be involved in doxorubicin-mediated DNA damage, was increased by doxorubicin treatment, but blocked by PKR inhibition. Protein translation was downregulated by doxorubicin treatment and upregulated by blocking PKR phosphorylation. These results suggest that PKR activation induces apoptosis by increasing the phosphorylation of eIF2α and CHK1 and decreasing the global protein translation in doxorubicin-treated HCC1143 triple-negative breast cancer cells. Full article
(This article belongs to the Special Issue New Insights into Overcoming Drug Resistance in Cancers)
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21 pages, 9233 KiB  
Article
Possible Mechanisms of Resistance Development to Photodynamic Therapy (PDT) In Vulvar Cancer Cells
by Beata Joanna Mossakowska, Anna Fabisiewicz, Barbara Tudek and Janusz Aleksander Siedlecki
Int. J. Mol. Sci. 2022, 23(23), 14689; https://doi.org/10.3390/ijms232314689 - 24 Nov 2022
Cited by 9 | Viewed by 1578
Abstract
Photodynamic therapy (PDT) is a low-invasive treatment method that can be used to treat VIN patients. A photosensitizer (PS) applied to a patient is activated with use of the appropriate wavelength of light, which in an oxygen environment leads to the formation of [...] Read more.
Photodynamic therapy (PDT) is a low-invasive treatment method that can be used to treat VIN patients. A photosensitizer (PS) applied to a patient is activated with use of the appropriate wavelength of light, which in an oxygen environment leads to the formation of a reactive oxygen species (ROS) that destroys the tumor. However, cells can protect themselves against these cytotoxic products by increasing their antioxidant mechanisms and repair capacity. Changes in the cytoskeleton may also influence resistance to PDT. Our results revealed that PDT-resistant cells changed the amount of ROS. Cells resistant to PDT A-431 exhibited a decreased ROS level and showed higher viability after oxidizing agent treatment. Resistant Cal-39 cells exhibited a decreased O2− level but increased other ROS. This provides protection from PDT but not from other oxidizing agents. Moreover, PDT leads to alterations in the cytoskeleton that may result in an epithelial-mesenchymal transition (EMT) or increased adhesion. Both EMT and cell adhesion may activate signaling pathways involved in survival. This means that resistance to PDT in vulvar cancer may be at least in part a result of changes in ROS level and alterations in the cytoskeleton. Full article
(This article belongs to the Special Issue New Insights into Overcoming Drug Resistance in Cancers)
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