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Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action

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

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 34299

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Dr. Simon J. Allison

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School of Applied Sciences, University of Huddersfield, Huddersfield HD1 3DH, UK
Interests: cancer metabolism; NAD⁺ biology; sirtuins; cancer selectivity; novel targets; target deconvolution

Special Issue Information

Dear Colleagues,

The focus of this Special Issue is “Novel Anti-Cancer Agents and Cellular Targets and Their Mechanism(s) of Action”. Whilst there have been significant improvements in treatments and outcomes for some cancers, for others there has been little change in survival rates over many years. Side effects resulting from the toxicity of agents towards normal tissues and the development of drug resistance can be a problem with both targeted and traditional anti-cancer agents. There is a pressing need for new anti-cancer agents with novel mechanism(s) of action and the identification of new putative cellular targets and therapeutic strategies that are both potent and more selective towards cancer cells. This Special Issue invites submissions in any area relating to these themes. Possible topics within this scope include (but are not limited to) the following:

New promising compounds with in vitro and/or in vivo anti-cancer activity identified through a phenotypic approach, and studies on elucidating their mechanism(s) of action;
New putative cellular targets that may offer cancer selectivity to targeting approaches (targeted therapies);
Novel therapeutic approaches, such as combinatorial chemotherapy, that may confer synthetic lethality or improve selectivity;
Drug re-purposing;
Promising agents showing polypharmacology;
Target deconvolution and target validation studies.

We invite authors to submit original research articles or review articles.

Dr. Simon J Allison
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 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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

novel cellular anti-cancer targets
phenotypic screening
novel anti-cancer agents
target deconvolution
polypharmacology
targeted therapies
drug re-purposing
combinatorial chemotherapy
target validation

Published Papers (11 papers)

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Editorial

Jump to: Research, Review

3 pages, 172 KiB

Open AccessEditorial

Novel Anti-Cancer Agents and Cellular Targets and Their Mechanism(s) of Action

by Simon J. Allison

Biomedicines 2022, 10(8), 1767; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10081767 - 22 Jul 2022

Viewed by 1239

Abstract

Whilst there have been some significant improvements in treatments and patient outcomes for some cancers, for other cancers there has been little change in survival rates for many years [...] Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

Research

Jump to: Editorial, Review

19 pages, 2639 KiB

Open AccessArticle

Targeting Tumor Cells Overexpressing the Human Epidermal Growth Factor Receptor 3 with Potent Drug Conjugates Based on Affibody Molecules

by Sara S. Rinne, Wen Yin, Anna Mestre Borras, Ayman Abouzayed, Charles Dahlsson Leitao, Anzhelika Vorobyeva, John Löfblom, Stefan Ståhl, Anna Orlova and Torbjörn Gräslund

Biomedicines 2022, 10(6), 1293; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10061293 - 31 May 2022

Cited by 3 | Viewed by 2171

Abstract

Increasing evidence suggests that therapy targeting the human epidermal growth factor receptor 3 (HER3) could be a viable route for targeted cancer therapy. Here, we studied a novel drug conjugate, Z_HER3-ABD-mcDM1, consisting of a HER3-targeting affibody molecule, coupled to the cytotoxic tubulin polymerization inhibitor DM1, and an albumin-binding domain for in vivo half-life extension. Z_HER3-ABD-mcDM1 showed a strong affinity to the extracellular domain of HER3 (K_D 6 nM), and an even stronger affinity (K_D 0.2 nM) to the HER3-overexpressing pancreatic carcinoma cell line, BxPC-3. The drug conjugate showed a potent cytotoxic effect on BxPC-3 cells with an IC₅₀ value of 7 nM. Evaluation of a radiolabeled version, [^99mTc]Tc-Z_HER3-ABD-mcDM1, showed a relatively high rate of internalization, with a 27% internalized fraction after 8 h. Further in vivo evaluation showed that it could target BxPC-3 (pancreatic carcinoma) and DU145 (prostate carcinoma) xenografts in mice, with an uptake peaking at 6.3 ± 0.4% IA/g at 6 h post-injection for the BxPC-3 xenografts. The general biodistribution showed uptake in the liver, lung, salivary gland, stomach, and small intestine, organs known to express murine ErbB3 naturally. The results from the study show that Z_HER3-ABD-mcDM1 is a highly potent and selective drug conjugate with the ability to specifically target HER3 overexpressing cells. Further pre-clinical and clinical development is discussed. Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

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16 pages, 4201 KiB

Open AccessArticle

Optically Coupled PtOEP and DPA Molecules Encapsulated into PLGA-Nanoparticles for Cancer Bioimaging

by Olena Vepris, Christina Eich, Yansong Feng, Gastón Fuentes, Hong Zhang, Eric L. Kaijzel and Luis J. Cruz

Biomedicines 2022, 10(5), 1070; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10051070 - 05 May 2022

Cited by 5 | Viewed by 2508

Abstract

Triplet-triplet annihilation upconversion (TTA-UC) nanoparticles (NPs) have emerged as imaging probes and therapeutic probes in recent years due to their excellent optical properties. In contrast to lanthanide ion-doped inorganic materials, highly efficient TTA-UC can be generated by low excitation power density, which makes it suitable for clinical applications. In the present study, we used biodegradable poly(lactic-co-glycolic acid) (PLGA)-NPs as a delivery vehicle for TTA-UC based on the heavy metal porphyrin Platinum(II) octaethylporphyrin (PtOEP) and the polycyclic aromatic hydrocarbon 9,10-diphenylanthracene (DPA) as a photosensitizer/emitter pair. TTA-UC-PLGA-NPs were successfully synthesized according to an oil-in-water emulsion and solvent evaporation method. After physicochemical characterization, UC-efficacy of TTA-UC-PLGA-NPs was assessed in vitro and ex vivo. TTA-UC could be detected in the tumour area 96 h after in vivo administration of TTA-UC-PLGA-NPs, confirming the integrity and suitability of PLGA-NPs as a TTA-UC in vivo delivery system. Thus, this study provides proof-of-concept that the advantageous properties of PLGA can be combined with the unique optical properties of TTA-UC for the development of advanced nanocarriers for simultaneous in vivo molecular imaging and drug delivery. Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

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21 pages, 4442 KiB

Open AccessArticle

Anticancer Effects with Molecular Docking Confirmation of Newly Synthesized Isatin Sulfonamide Molecular Hybrid Derivatives against Hepatic Cancer Cell Lines

by Mahmoud Eldeeb, Eman F. Sanad, Ahmed Ragab, Yousry A. Ammar, Khaled Mahmoud, Mamdouh M. Ali and Nadia M. Hamdy

Biomedicines 2022, 10(3), 722; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10030722 - 20 Mar 2022

Cited by 36 | Viewed by 4073

Abstract

The current study investigated the cytotoxic effect of ten sulfonamide-derived isatins, following molecular hybridization, based on the association principles, on hepatocellular carcinoma (HCC) HepG2 and Huh7 cell lines, compared for safety using human normal retina pigmented epithelial (RPE-1) cells. The ten compounds showed variable in vitro cytotoxicity on HepG2 and Huh7 cells, using the MTT assay. Four compounds (4/10) were highly cytotoxic to both HepG2 and HuH7. However, only 3 of these 4 were of the highest safety margin on RPE-1 cells in vitro and in the in vivo acute (14-day) oral toxicity study. These later, superior three compounds’ structures are 3-hydroxy-3-(2-oxo-2-(p-tolyl)ethyl)-5-(piperidin-1-ylsulfonyl)indolin-2-one (3a), N-(4-(2-(2-oxo-5-(piperidin-1-ylsulfonyl)indolin-3-ylidene)acetyl)phenyl)acetamide (4b), and N-(3-(2-(2-oxo-5-(piperidin-1-ylsulfonyl)indolin-3-ylidene)acetyl)phenyl)acetamide (4c). The half-maximal inhibitory concentration (IC50) of the tested compounds (3a, 4b, and 4c) on HepG2 cells were approximately 16.8, 44.7, and 39.7 μM, respectively. The 3a, 4b, and 4c compounds significantly decreased the angiogenic marker epithelial growth factor receptor (EGFR) level and that was further confirmed via molecular docking inside the EFGR active site (PDB: 1M17). The binding free energies ranged between −19.21 and −21.74 Kcal/mol compared to Erlotinib (−25.65 Kcal/mol). The most promising compounds, 3a, 4b, and 4c, showed variable anticancer potential on “hallmarks of cancer”, significant cytotoxicity, and apoptotic anti-angiogenic and anti-invasive effects, manifested as suppression of Bcl-2, urokinase plasminogen activation, and heparanase expression in HepG2-treated cells’ lysate, compared to non-treated HepG2 cells. In conclusion, compound “3a” is highly comparable to doxorubicin regarding cell cycle arrest at G2/M, the pre-G0 phases and early and late apoptosis induction and is comparable to Erlotinib regarding binding to EGFR active site. Therefore, the current study could suggest that compound “3a” is, hopefully, the most safe and active synthesized isatin sulfonamide derivative for HCC management. Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

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16 pages, 6050 KiB

Open AccessArticle

Drug Resistance in Glioma Cells Induced by a Mesenchymal–Amoeboid Migratory Switch

by Sophie E. Ketchen, Filomena O. Gamboa-Esteves, Sean E. Lawler, Michal O. Nowicki, Arndt Rohwedder, Sabine Knipp, Sally Prior, Susan C. Short, John E. Ladbury and Anke Brüning-Richardson

Biomedicines 2022, 10(1), 9; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10010009 - 22 Dec 2021

Cited by 6 | Viewed by 3371

Abstract

Cancer cell invasion is a precondition for tumour metastasis and represents one of the most devastating characteristics of cancer. The development of drugs targeting cell migration, known as migrastatics, may improve the treatment of highly invasive tumours such as glioblastoma (GBM). In this study, investigations into the role of the cell adhesion protein Cellular communication network factor 1 (CCN1, also known as CYR61) in GBM cell migration uncovered a drug resistance mechanism adopted by cells when treated with the small molecule inhibitor CCG-1423. This inhibitor binds to importin α/β inhibiting the nuclear translocation of the transcriptional co-activator MKL1, thus preventing downstream effects including migration. Despite this reported role as an inhibitor of cell migration, we found that CCG-1423 treatment did not inhibit GBM cell migration. However, we could observe cells now migrating by mesenchymal–amoeboid transition (MAT). Furthermore, we present evidence that CCN1 plays a critical role in the progression of GBM with increased expression in higher-grade tumours and matched blood samples. These findings support a potential role for CCN1 as a biomarker for the monitoring and potentially early prediction of GBM recurrence, therefore as such could help to improve treatment of and increase survival rates of this devastating disease. Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

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25 pages, 5723 KiB

Open AccessArticle

Cytocidal Antitumor Effects against Human Ovarian Cancer Cells Induced by B-Lactam Steroid Alkylators with Targeted Activity against Poly (ADP-Ribose) Polymerase (PARP) Enzymes in a Cell-Free Assay

by Nikolaos Nikoleousakos, Panagiotis Dalezis, Aikaterini Polonifi, Elena G. Geromichalou, Sofia Sagredou, Constantinos E. Alifieris, Maria V. Deligiorgi, Vasiliki Sarli and Dimitrios T. Trafalis

Biomedicines 2021, 9(8), 1028; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9081028 - 17 Aug 2021

Cited by 2 | Viewed by 2320

Abstract

We evaluated three newly synthesized B-lactam hybrid homo-aza-steroidal alkylators (ASA-A, ASA-B and ASA-C) for their PARP1/2 inhibition activity and their DNA damaging effect against human ovarian carcinoma cells. These agents are conjugated with an alkylating component (POPA), which also served as a reference molecule (positive control), and were tested against four human ovarian cell lines in vitro (UWB1.289 + BRCA1, UWB1.289, SKOV-3 and OVCAR-3). The studied compounds were thereafter compared to 3-AB, a known PARP inhibitor, as well as to Olaparib, a standard third-generation PARP inhibitor, on a PARP assay investigating their inhibitory potential. Finally, a PARP1 and PARP2 mRNA expression analysis by qRT-PCR was produced in order to measure the absolute and the relative gene expression (in mRNA transcripts) between treated and untreated cells. All the investigated hybrid steroid alkylators and POPA decreased in vitro cell growth differentially, according to the sensitivity and different gene characteristics of each cell line, while ASA-A and ASA-B presented the most significant anticancer activity. Both these compounds induced PARP1/2 enzyme inhibition, DNA damage (alkylation) and upregulation of PARP mRNA expression, for all tested cell lines. However, ASA-C underperformed on average in the above tasks, while the compound ASA-B induced synthetic lethality effects on the ovarian cancer cells. Nevertheless, the overall outcome, leading to a drug-like potential, provides strong evidence toward further evaluation. Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

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13 pages, 2329 KiB

Open AccessArticle

Predicting Agents That Can Overcome 5-FU Resistance in Colorectal Cancers via Pharmacogenomic Analysis

by Tsui-Chin Huang, Kuan-Chieh Peng, Tzu-Ting Kuo, Li-Chun Lin, Bai-Chia Liu, Shu-Ping Ye, Chien-Chou Chu, Shih-Min Hsia and Hsin-Yi Chang

Biomedicines 2021, 9(8), 882; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9080882 - 24 Jul 2021

Cited by 5 | Viewed by 2332

Abstract

5-Fluorouracil (5-FU) is one of several chemotherapeutic agents in clinical use as a standard of care to treat colorectal cancers (CRCs). As an antimetabolite, 5-FU inhibits thymidylate synthase to disrupt the synthesis and repair of DNA and RNA. However, only a small proportion of patients benefit from 5-FU treatment due to the development of drug resistance. This study applied pharmacogenomic analysis using two public resources, the Genomics of Drug Sensitivity in Cancer (GDSC) and the Connectivity Map, to predict agents overcoming 5-FU resistance in CRC cells based on their genetic background or gene expression profile. Based on the genetic status of adenomatous polyposis coli (APC), the most frequent mutated gene found in CRC, we found that combining a MEK inhibitor with 5-FU exhibited synergism effects on CRC cells with APC truncations. While considering the gene expression in 5-FU resistant cells, we demonstrated that targeting ROCK is a potential avenue to restore 5-FU response to resistant cells with wild-type APC background. Our results reveal MEK signaling plays a pivotal role in loss-of-function, APC-mediated 5-FU resistance, and ROCK activation serves as a signature in APC-independent 5-FU resistance. Through the use of these available database resources, we highlight possible approaches to predict potential drugs for combinatorial therapy for patients developing resistance to 5-FU treatment. Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

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23 pages, 4919 KiB

Open AccessEditor’s ChoiceArticle

8-Hydroxydaidzein, an Isoflavone from Fermented Soybean, Induces Autophagy, Apoptosis, Differentiation, and Degradation of Oncoprotein BCR-ABL in K562 Cells

by Pei-Shan Wu, Jui-Hung Yen, Chih-Yang Wang, Pei-Yi Chen, Jui-Hsiang Hung and Ming-Jiuan Wu

Biomedicines 2020, 8(11), 506; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8110506 - 16 Nov 2020

Cited by 17 | Viewed by 3045

Abstract

8-Hydroxydaidzein (8-OHD, 7,8,4′-trihydoxyisoflavone) is a hydroxylated derivative of daidzein isolated from fermented soybean products. The aim of this study is to investigate the anti-proliferative effects and the underlying mechanisms of 8-OHD in K562 human chronic myeloid leukemia (CML) cells. We found that 8-OHD induced reactive oxygen species (ROS) overproduction and cell cycle arrest at the S phase by upregulating p21^Cip1 and downregulating cyclin D2 (CCND2) and cyclin-dependent kinase 6 (CDK6) expression. 8-OHD also induced autophagy, caspase-7-dependent apoptosis, and the degradation of BCR-ABL oncoprotein. 8-OHD promoted Early Growth Response 1 (EGR1)-mediated megakaryocytic differentiation as an increased expression of marker genes, CD61 and CD42b, and the formation of multi-lobulated nuclei in enlarged K562 cells. A microarray-based transcriptome analysis revealed a total of 3174 differentially expressed genes (DEGs) after 8-OHD (100 μM) treatment for 48 h. Bioinformatics analysis of DEGs showed that hemopoiesis, cell cycle regulation, nuclear factor-κB (NF-κB), and mitogen-activated protein kinase (MAPK) and Janus kinase/signal transducers and activators of transcription (JAK-STAT)-mediated apoptosis/anti-apoptosis networks were significantly regulated by 8-OHD. Western blot analysis confirmed that 8-OHD significantly induced the activation of MAPK and NF-κB signaling pathways, both of which may be responsible, at least in part, for the stimulation of apoptosis, autophagy, and differentiation in K562 cells. This is the first report on the anti-CML effects of 8-OHD and the combination of experimental and in silico analyses could provide a better understanding for the development of 8-OHD on CML therapy. Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

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16 pages, 3628 KiB

Open AccessArticle

Potent Small-Molecule Inhibitors Targeting Acetylated Microtubules as Anticancer Agents Against Triple-Negative Breast Cancer

by Ahreum Kwon, Gwi Bin Lee, Taein Park, Jung Hoon Lee, Panseon Ko, Eunae You, Jin Hee Ahn, Soo Hyun Eom, Sangmyung Rhee and Woo Keun Song

Biomedicines 2020, 8(9), 338; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8090338 - 09 Sep 2020

Cited by 9 | Viewed by 3142

Abstract

Microtubules are one of the major targets for anticancer drugs because of their role in cell proliferation and migration. However, as anticancer drugs targeting microtubules have side effects, including the death of normal cells, it is necessary to develop anticancer agents that can target microtubules by specifically acting on cancer cells only. In this study, we identified chemicals that can act as anticancer agents by specifically binding to acetylated microtubules, which are predominant in triple-negative breast cancer (TNBC). The chemical compounds disrupted acetylated microtubule lattices by interfering with microtubule access to alpha-tubulin acetyltransferase 1 (αTAT1), a major acetyltransferase of microtubules, resulting in the increased apoptotic cell death of MDA-MB-231 cells (a TNBC cell line) compared with other cells, such as MCF-10A and MCF-7, which lack microtubule acetylation. Moreover, mouse xenograft experiments showed that treatment with the chemical compounds markedly reduced tumor growth progression. Taken together, the newly identified chemical compounds can be selective for acetylated microtubules and act as potential therapeutic agents against microtubule acetylation enrichment in TNBC. Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

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Review

Jump to: Editorial, Research

22 pages, 3321 KiB

Open AccessReview

Intratumoural Cytochrome P450 Expression in Breast Cancer: Impact on Standard of Care Treatment and New Efforts to Develop Tumour-Selective Therapies

by Smarakan Sneha, Simon C. Baker, Andrew Green, Sarah Storr, Radhika Aiyappa, Stewart Martin and Klaus Pors

Biomedicines 2021, 9(3), 290; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9030290 - 12 Mar 2021

Cited by 22 | Viewed by 4636

Abstract

Despite significant advances in treatment strategies over the past decade, selective treatment of breast cancer with limited side-effects still remains a great challenge. The cytochrome P450 (CYP) family of enzymes contribute to cancer cell proliferation, cell signaling and drug metabolism with implications for treatment outcomes. A clearer understanding of CYP expression is important in the pathogenesis of breast cancer as several isoforms play critical roles in metabolising steroid hormones and xenobiotics that contribute to the genesis of breast cancer. The purpose of this review is to provide an update on how the presence of CYPs impacts on standard of care (SoC) drugs used to treat breast cancer as well as discuss opportunities to exploit CYP expression for therapeutic intervention. Finally, we provide our thoughts on future work in CYP research with the aim of supporting ongoing efforts to develop drugs with improved therapeutic index for patient benefit. Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

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15 pages, 1193 KiB

Open AccessReview

Anti-c-myc RNAi-Based Onconanotherapeutics

by Saffiya Habib, Mario Ariatti and Moganavelli Singh

Biomedicines 2020, 8(12), 612; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8120612 - 15 Dec 2020

Cited by 13 | Viewed by 3301

Abstract

Overexpression of the c-myc proto-oncogene features prominently in most human cancers. Early studies established that inhibiting the expression of oncogenic c-myc, produced potent anti-cancer effects. This gave rise to the notion that an appropriate c-myc silencing agent might provide a broadly applicable and more effective form of cancer treatment than is currently available. The endogenous mechanism of RNA interference (RNAi), through which small RNA molecules induce gene silencing by binding to complementary mRNA transcripts, represents an attractive avenue for c-myc inhibition. However, the development of a clinically viable, anti-c-myc RNAi-based platform is largely dependent upon the design of an appropriate carrier of the effector nucleic acids. To date, organic and inorganic nanoparticles were assessed both in vitro and in vivo, as carriers of small interfering RNA (siRNA), DICER-substrate siRNA (DsiRNA), and short hairpin RNA (shRNA) expression plasmids, directed against the c-myc oncogene. We review here the various anti-c-myc RNAi-based nanosystems that have come to the fore, especially between 2005 and 2020. Full article

(This article belongs to the Special Issue Novel Anti-cancer Agents and Cellular Targets and Their Mechanism(s) of Action)

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