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The Role of Natural Compounds in Cancer Therapy
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The Role of Natural Compounds in Cancer Therapy

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 4163

Special Issue Editor

Prof. Dr. Alok Bhushan

E-Mail Website
Guest Editor
Département of Pharmaceutical Sciences, Jefferson Collège of Pharmacy, Thomas Jefferson University, Philadelphia, PA 19107, USA
Interests: cancer chemotherapy; pharmacology; signal transduction; invasion; combination therapy; apoptosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

A significant number of small-molecule medicines that are used today for the treatment of cancer are natural products or derivatives of natural products. Natural products are bioactive compounds that affect cellular processes including cell metabolism, signaling, and transcription. Advancements in new technologies have been critical in the development of antibody-based therapies. These antibodies bind specific proteins in the cancer cells to affect the activity of specific cancer-causing elements and are also used in targeting specific cancer cells to deliver drugs by designing antibodies with conjugated small molecules.  Chemotherapy using small molecules still remains an approach to treat cancer patients successfully. The mechanisms of the drugs may be altered by natural compounds by affecting cellular processes as well as metabolism, which would affect the outcome of the successful chemotherapy. The natural compounds may also affect the efficacy of the drugs as well as the development of resistance.

This Special Issue invites papers and reviews that add to our knowledge regarding the effects of various natural products on cellular processes and their impact on treatments with current therapies at the molecular level. Submissions can include combination therapies with natural products as well as the repurposing of currently known drugs.

Prof. Dr. Alok Bhushan
Guest Editor

Manuscript Submission Information

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Keywords

  • natural compounds
  • cancer
  • repurposing
  • combination
  • polychemotherapy
  • pharmaceuticals
  • nutraceuticals
  • molecular targets
  • metabolism
  • metabolomics
  • enhancing efficacy
  • immunotherapy

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Published Papers (5 papers)

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Research

16 pages, 3123 KiB  
Article
Anticancer Activity of Ethyl Acetate/Water Fraction from Tanacetum vulgare L. Leaf and Flower Extract
by Inna Sulikovska, Ani Georgieva, Vera Djeliova, Katerina Todorova, Anelia Vasileva, Ivaylo Ivanov and Mashenka Dimitrova
Curr. Issues Mol. Biol. 2025, 47(4), 215; https://doi.org/10.3390/cimb47040215 - 21 Mar 2025
Viewed by 249
Abstract
The present paper aims to assess the antitumor activity of ethyl acetate/water soluble fraction obtained from the extract of Tanacetum vulgare L. leaves and flowers (EATV). The chemical composition of EATV was determined by LC-HPMS. In vitro studies were performed on the HT-29 [...] Read more.
The present paper aims to assess the antitumor activity of ethyl acetate/water soluble fraction obtained from the extract of Tanacetum vulgare L. leaves and flowers (EATV). The chemical composition of EATV was determined by LC-HPMS. In vitro studies were performed on the HT-29 cell line (human colorectal carcinoma). The effect on the cell cycle and the pro-apoptotic activity were evaluated using flow cytometry analyses. Genotoxicity was analyzed by the comet assay. In vivo antitumor potential of EATV was assessed in Ehrlich’s tumor-bearing mice. Pathological, histological, and hematological analyses of the EATV-treated animals were performed, and the effect of the treatment on the lifespan was evaluated. The LC-HRMS analysis demonstrated a complex phytochemical profile of EATV comprising more than forty compounds, thirty-six of which were identified. The results showed that the antitumor activity of EATV towards HT-29 cells is due to a pronounced genotoxicity leading to cell cycle arrest and apoptosis of the cells. Pathological studies revealed more massive and frequently detected tumor necrosis, apoptosis, and fistulation in T. vulgare-treated mice compared to positive tumor-bearing controls. Furthermore, it was demonstrated that the intraperitoneal application of EATV prolonged the animal’s lifespan. Full article
(This article belongs to the Special Issue The Role of Natural Compounds in Cancer Therapy)
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18 pages, 12773 KiB  
Article
Lycobetaine Has Therapeutic Efficacy in Lung Squamous Cell Carcinoma by Targeting USP32 to Trigger Ferroptosis
by Shangping Xing, Hua Chai, Zhenlong Chen, Shuye Deng and Feifei Nong
Curr. Issues Mol. Biol. 2025, 47(3), 163; https://doi.org/10.3390/cimb47030163 - 27 Feb 2025
Viewed by 540
Abstract
Ubiquitin-specific protease 32 (USP32), a deubiquitylating enzyme that controls the ubiquitin process, is overexpressed in multiple cancers and serves as a promising therapeutic target for cancer therapy. Drugs targeting ferroptosis have exhibited promising anticancer activity. Lycobetaine (LBT), a natural alkaloid, holds promise against [...] Read more.
Ubiquitin-specific protease 32 (USP32), a deubiquitylating enzyme that controls the ubiquitin process, is overexpressed in multiple cancers and serves as a promising therapeutic target for cancer therapy. Drugs targeting ferroptosis have exhibited promising anticancer activity. Lycobetaine (LBT), a natural alkaloid, holds promise against various cancers, yet its specific targets and anticancer mechanisms remain unclear. In this study, we show that LBT induced ferroptosis in lung squamous cell carcinoma (LUSC) cells, accompanied by glutathione depletion and the accumulation of lipid peroxidation, malondialdehyde, and ferrous iron. Mechanistically, drug affinity responsive target stability-based mass spectrometry analysis, molecular dynamics simulations, and a cellular thermal shift assay confirmed that USP32 is a potential target of LBT in LUSC cells. Moreover, a strong interaction between USP32 and nuclear factor erythroid 2-related factor 2 (NRF2) was found via immunoprecipitation–mass spectrometry and co-immunoprecipitation. In addition, the ubiquitination assay results demonstrated that LBT treatment significantly increased NRF2 ubiquitination and degradation by targeting USP32. Importantly, USP32 overexpression effectively attenuated the effects of LBT on proliferation and ferroptosis in LUSC cells. In orthotopic LUSC xenografts, the administration of LBT significantly inhibited tumor growth and metastasis and induced ferroptosis by targeting the USP32–NRF2 signaling axis. Taken together, these data suggest that LBT exerts its anticancer effects by inhibiting USP32-mediated NRF2 deubiquitination to induce ferroptosis and that LBT may serve as a prospective USP32-targeting agent for LUSC treatment. Full article
(This article belongs to the Special Issue The Role of Natural Compounds in Cancer Therapy)
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21 pages, 2703 KiB  
Article
Gallic Acid Enhances Olaparib-Induced Cell Death and Attenuates Olaparib Resistance in Human Osteosarcoma U2OS Cell Line
by Mehmet Kadir Erdogan and Ayse Busra Usca
Curr. Issues Mol. Biol. 2025, 47(2), 104; https://doi.org/10.3390/cimb47020104 - 7 Feb 2025
Viewed by 976
Abstract
Cancer remains one of the most formidable diseases globally and continues to be a leading cause of mortality. While chemotherapeutic agents are crucial in cancer treatment, they often come with severe side effects. Furthermore, the development of acquired drug resistance poses a significant [...] Read more.
Cancer remains one of the most formidable diseases globally and continues to be a leading cause of mortality. While chemotherapeutic agents are crucial in cancer treatment, they often come with severe side effects. Furthermore, the development of acquired drug resistance poses a significant challenge in the ongoing battle against cancer. Combining these chemotherapeutic agents with plant-derived phenolic compounds offers a promising approach, potentially reducing side effects and counteracting drug resistance. Phytochemicals, the bioactive compounds found in plants, exhibit a range of health-promoting properties, including anticarcinogenic, antimutagenic, antiproliferative, antioxidant, antimicrobial, neuroprotective, and cardioprotective effects. Their ability to enhance treatment, coupled with their non-toxic, multi-targeted nature and synergistic potential when used alongside conventional drugs, underscores the growing importance of natural therapeutics. In this study, we investigated the anticancer effects of olaparib (OL), a small-molecule PARP inhibitor that has shown promising results in both preclinical and clinical trials, and gallic acid (GA), a phenolic compound, in olaparib-resistant human osteosarcoma U2OS cells (U2OS-PIR). Both parental U2OS and U2OS-PIR cell lines were treated with increasing concentrations of olaparib and gallic acid, and their cytotoxic effects were assessed using the WST-1 cell viability assay. The synergistic potential of OL and GA, based on their determined IC50 values, was further explored in combination treatment. A colony survival assay revealed the combination’s ability to significantly reduce the colony-forming capacity of cancer cells. Additionally, the apoptotic effects of OL and GA, both individually and in combination, were examined in U2OS-PIR cells using acridine orange/ethidium bromide dual staining. The anti-angiogenic properties were assessed through a VEGF ELISA, while the expression of proteins involved in DNA damage and apoptotic signaling pathways was analyzed via Western blot. The results of this study demonstrate that gallic acid effectively suppresses cell viability and colony formation, particularly when used in combination therapy to combat OL resistance. Additionally, GA inhibits angiogenesis and induces DNA damage and apoptosis by modulating key apoptosis-related proteins, including cPARP, Bcl-2, and Bax. These findings highlight gallic acid as a potential compound for enhancing therapeutic efficacy in overcoming acquired drug resistance. Full article
(This article belongs to the Special Issue The Role of Natural Compounds in Cancer Therapy)
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13 pages, 1918 KiB  
Article
Screening of the Antimelanoma Activity of Monoterpenes—In Vitro Experiments on Four Human Melanoma Lines
by Paula Wróblewska-Łuczka, Laura Kulenty, Katarzyna Załuska-Ogryzek, Agnieszka Góralczyk and Jarogniew J. Łuszczki
Curr. Issues Mol. Biol. 2025, 47(2), 97; https://doi.org/10.3390/cimb47020097 - 3 Feb 2025
Cited by 1 | Viewed by 765
Abstract
(1) Malignant melanoma is the most aggressive type of malignant tumor caused by a dysfunction of melanocytes. Despite progress in the treatment of melanoma, further research and search for new potential drugs are necessary to optimize the therapy. (2) The aim of this [...] Read more.
(1) Malignant melanoma is the most aggressive type of malignant tumor caused by a dysfunction of melanocytes. Despite progress in the treatment of melanoma, further research and search for new potential drugs are necessary to optimize the therapy. (2) The aim of this study was to evaluate the antiproliferative activity of eight selected monoterpenes by MTT and LDH assays on four malignant melanoma cell lines. (3) Myrcene, rhodinol and nerol did not show any significant anticancer effect on melanoma cell lines, but citral, carvacrol, citronellol, thymol and geraniol showed a significant anti-viability effect. Our studies have shown that the most effective terpene among those tested in inhibiting melanoma cell viability was carvacrol, with the lowest IC50 in the range of 0.05 ± 0.00 to 0.06 ± 0.01 mM. Moreover, it did not negatively affect normal human keratinocyte cells. (4) Metastatic melanoma is very difficult to treat, and some terpenes have the ability to sensitize cells to other chemicals; so, it is worth investigating their antimelanoma potential, as terpenes could become an adjuvant to traditional treatment. Full article
(This article belongs to the Special Issue The Role of Natural Compounds in Cancer Therapy)
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11 pages, 1472 KiB  
Article
Exploring the Anticancer Potential of MonoHER (7-Mono-O-(β-Hydroxyethyl)-Rutoside): Mitochondrial-Dependent Apoptosis in HepG2 Cells
by Chujie Li, Yue Wang, Jian Liang, Guido R. M. M. Haenen, Yonger Chen, Zhengwen Li, Ming Zhang and Ludwig J. Dubois
Curr. Issues Mol. Biol. 2025, 47(1), 36; https://doi.org/10.3390/cimb47010036 - 9 Jan 2025
Viewed by 912
Abstract
Background/Aim: Flavonoids are a group of polyphenols, abundantly present in our diet. Although, based on their chemoprotective effects, intake of flavonoids is associated with a high anticancer potential as evidenced in in vitro and in vivo models, the molecular mechanism is still elusive. [...] Read more.
Background/Aim: Flavonoids are a group of polyphenols, abundantly present in our diet. Although, based on their chemoprotective effects, intake of flavonoids is associated with a high anticancer potential as evidenced in in vitro and in vivo models, the molecular mechanism is still elusive. This study explores the antiproliferative and cytotoxic effects of the semi-synthetic flavonoid MonoHER (7-mono-O-(β-hydroxyethyl)-rutoside) in vitro on cancer cells. Materials and Methods: HepG2 liver, MCF7 breast, and H1299 lung cancer cells were grown under ambient conditions with or without MonoHER exposure. CCK8 assay was used to assess cell viability. Apoptosis, JC-1, and mitochondrial mass were determined using flow cytometry and confocal analysis. The effects of monoHER on apoptosis proteins were detected by confocal microscopy analysis and Western blot. Results: It was found that MonoHER can reduce HepG2 cells’ and MCF7 cells’ viability, but not H1299 cells’, and induced apoptosis only in HepG2 cells. MonoHER has the potential to enhance the expression of caspase-9 and caspase-3, to damage mitochondria, and to provoke the release of cytochrome C from the mitochondria. Conclusion: MonoHER can inhibit cell growth and induce apoptosis especially in HepG2 human liver cancer cells by triggering the mitochondrial signal transduction pathway, leading to the release of cytochrome C in the cytoplasm and the subsequent activation of caspase-9 and caspase-3. Future research should further explore MonoHER’s mechanism of action, efficacy, and potential for clinical translation. Full article
(This article belongs to the Special Issue The Role of Natural Compounds in Cancer Therapy)
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