Cancer Molecular Biology and Drug Discovery

A special issue of BioChem (ISSN 2673-6411).

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 3230

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Guest Editor
Graduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan
Interests: cancer biology; bioinformatics; drug repurposing
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Special Issue Information

Dear Colleagues,

Cancer is a major health issue worldwide, with an increasing global burden in the coming years. Some malignancies, such as colorectal, breast, prostate, and pancreatic cancers, are still incurable in advanced stages. Thus, more effective anticancer drugs are always urgently needed. The process of drug discovery is still risky, lengthy, and costly, and only a few new anticancer drugs have received approval in recent years. Drug repurposing is an unconventional drug discovery approach to explore new disease indications from existing clinical drugs. Even shelved drugs that never enter or fail during clinical trials might be rescued if novel mechanisms of action (MOAs) or targets are identified. Polypharmacology describes the ability of a drug to affect more than one molecular target, which is now commonly accepted as a basic property of small molecules and serves as a foundational principle for drug repurposing. Exploring polypharmacology is highly useful for discovering drugs’ novel MOAs to improve their therapeutic efficacies and treat different diseases. The advantages of drug repurposing include a reduction in cost and the bypass of safety concerns because extensive drug data are often available.

This Special Issue will focus on the development of novel cancer therapy based on polypharmacology and drug repurposing strategies. We welcome original research articles and review articles in this field.

Dr. Pei-Ming Yang
Guest Editor

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Keywords

  • cancer therapy
  • cancer biology
  • drug discovery
  • drug repurposing
  • polypharmacology

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Published Papers (2 papers)

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Research

19 pages, 3037 KiB  
Article
Tillandsia usneoides Ethanolic Extract Induces Cytotoxicity in SW480 Colon Cancer Cell Line via PPARγ Modulation
by María Paula López, María Camila Jiménez, Julián Esteban Contreras, Laura Rojas, Susana Fiorentino and José Iglesias
BioChem 2024, 4(3), 217-235; https://doi.org/10.3390/biochem4030011 - 26 Aug 2024
Viewed by 445
Abstract
Colorectal cancer (CRC) is a prevalent and deadly tumor worldwide. Understanding the molecular mechanisms underlying CRC development will improve treatment outcomes and patient survival. Natural molecules and metabolites from plants, such as Tillandsia usneoides, reduce tumor growth by modulating glucose metabolism and [...] Read more.
Colorectal cancer (CRC) is a prevalent and deadly tumor worldwide. Understanding the molecular mechanisms underlying CRC development will improve treatment outcomes and patient survival. Natural molecules and metabolites from plants, such as Tillandsia usneoides, reduce tumor growth by modulating glucose metabolism and increasing reactive oxygen species (ROS). To shed light on the mechanism involved in the anti-tumor effects of T. usneoides, we evaluated the cytotoxic effect of the ethanolic extract of this plant on the colon cancer cell line SW480 through the activation of the peroxisome proliferator-activated receptor gamma (PPARγ), a nuclear receptor that plays a role on lipid metabolism and inflammation in cancer cells. To this end, we assessed the activation of PPARγ by T. usneoides extract in transactivation luciferase assays, as well as the cytotoxic effect of this extract on the SW480 cell line after knocking down PPARγ using shRNA. Our findings indicate that the T. usneoides extract exhibits cytotoxic effects on the SW480 cell line, potentially in the same way as PPARγ activator, pioglitazone, i.e., by increasing reactive oxygen species (ROS). In addition, both T. usneoides extract and pioglitazone exert lipogenic properties in the SW480 cells. Taken together, these results demonstrate that the T. usneoides extract decreases the viability of the colon cancer cell line SW480, at least in part, through the activation of PPARγ. This suggests the potential for further use of this plant in the treatment of other chronic diseases. Full article
(This article belongs to the Special Issue Cancer Molecular Biology and Drug Discovery)
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17 pages, 3402 KiB  
Article
Fluorinated Derivatives of Digalloyl-Flavan-3-ol Induce Autophagic Cell Death by Forming Granular Aggregates Containing Mitochondria
by Ryo Doge, Yuki Nishino and Akiko Saito
BioChem 2023, 3(2), 61-77; https://doi.org/10.3390/biochem3020005 - 17 Apr 2023
Cited by 1 | Viewed by 1987
Abstract
Flavan-3-ol derivatives are polyphenolic compounds with multifunctional properties. One of the flavan-3-ol derivatives, green tea catechin epigallocatechin gallate, is known to have anticancer activity as one of its multifunctional properties. We have studied the synthesis of flavan-3-ol derivatives and conducted structure-activity relationship studies; [...] Read more.
Flavan-3-ol derivatives are polyphenolic compounds with multifunctional properties. One of the flavan-3-ol derivatives, green tea catechin epigallocatechin gallate, is known to have anticancer activity as one of its multifunctional properties. We have studied the synthesis of flavan-3-ol derivatives and conducted structure-activity relationship studies; we found that the fluorinated derivatives exhibited high toxicity against HeLa and A549 cells. It was confirmed that the cytotoxicity was affected by the conformation of the flavan-3-ol skeleton and that the 2,3-cis form was dominant. The addition of fluorinated compounds increased the amount of intracellular mitochondrial superoxide, abolished the membrane potential of mitochondria, and, interestingly, formed granular aggregates containing mitochondria. When the level of LC3-II, a marker of autophagy induction, was confirmed, it suggested that the addition of the fluorinated compounds promoted autophagy. These results suggest that the novel highly cytotoxic fluorinated flavan-3-ol compound synthesized in this study promotes autophagy and induces cell death by triggering mitochondrial dysfunction. We believe that these results suggest the possibility of conferring more functionality through structural transformations of flavan-3-ol derivatives. Full article
(This article belongs to the Special Issue Cancer Molecular Biology and Drug Discovery)
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