Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
6.7
4.6
Journals
Molecules
Special Issues
Anticancer Research: Towards an Understanding of Cancer and Discovery of...
molecules-logo
Submit to Molecules Review for Molecules Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Anticancer Research: Towards an Understanding of Cancer and Discovery of New Therapeutic Agents

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 6501

Special Issue Editors

Dr. Yu-shan Wu

E-Mail Website
Guest Editor
Department of Chemistry, Tunghai University, Taichung, Taiwan
Interests: medicinal chemistry; multidrug resistance; ABC transporters
Dr. Guor-Jien Wei

E-Mail Website
Guest Editor
Institute of Food Safety and Health Risk Assessment, National Yang Ming Chiao Tung University, Taipei, Taiwan
Interests: mass spectrometry; analytical chemistry; drug analysis; metabolimics; natural products

Special Issue Information

Dear Colleagues,

Cancer is one of the main causes of death worldwide. Over recent decades, advances in chemotherapy, targeted therapy, and immunotherapy have improved the prognosis of cancer patients significantly. The problem with treating cancer is that there are more than 200 different cancers resulting from different cellular defects and they often respond to therapeutic agents differently. The development of multidrug resistance and brain metathesis in cancer patients further complicates treatment. In this Special Issue, we welcome reviews and original research on various aspects of cancer, including the identification of novel natural/synthetic compounds with anticancer activity; the design of targeted therapeutic agents; the development of reversal agents for resistant cancer cells; and the design of agents/probes that elucidate mechanisms of action.

Dr. Yu-shan Wu
Dr. Guor-Jien Wei
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 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. Molecules 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 2700 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

  • anticancer agents
  • MDR reversal agents
  • targeted therapy
  • kinase inhibitors
  • chemical probe cancer

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

22 pages, 6534 KiB  
Article
Pan-EGFR Inhibitor Dacomitinib Resensitizes Paclitaxel and Induces Apoptosis via Elevating Intracellular ROS Levels in Ovarian Cancer SKOV3-TR Cells
by Ye Jin Lim, Hee Su Kim, Seunghee Bae, Kyeong A So, Tae Jin Kim and Jae Ho Lee
Molecules 2024, 29(1), 274; https://doi.org/10.3390/molecules29010274 - 4 Jan 2024
Viewed by 1311
Abstract
Paclitaxel is still used as a standard first-line treatment for ovarian cancer. Although paclitaxel is effective for many types of cancer, the emergence of chemoresistant cells represents a major challenge in chemotherapy. Our study aimed to analyze the cellular mechanism of dacomitinib, a [...] Read more.
Paclitaxel is still used as a standard first-line treatment for ovarian cancer. Although paclitaxel is effective for many types of cancer, the emergence of chemoresistant cells represents a major challenge in chemotherapy. Our study aimed to analyze the cellular mechanism of dacomitinib, a pan-epidermal growth factor receptor (EGFR) inhibitor, which resensitized paclitaxel and induced cell cytotoxicity in paclitaxel-resistant ovarian cancer SKOV3-TR cells. We investigated the significant reduction in cell viability cotreated with dacomitinib and paclitaxel by WST-1 assay and flow cytometry analysis. Dacomitinib inhibited EGFR family proteins, including EGFR and HER2, as well as its downstream signaling proteins, including AKT, STAT3, ERK, and p38. In addition, dacomitinib inhibited the phosphorylation of Bad, and combination treatment with paclitaxel effectively suppressed the expression of Mcl-1. A 2′-7′-dichlorodihydrofluorescein diacetate (DCFH-DA) assay revealed a substantial elevation in cellular reactive oxygen species (ROS) levels in SKOV3-TR cells cotreated with dacomitinib and paclitaxel, which subsequently mediated cell cytotoxicity. Additionally, we confirmed that dacomitinib inhibits chemoresistance in paclitaxel-resistant ovarian cancer HeyA8-MDR cells. Collectively, our research indicated that dacomitinib effectively resensitized paclitaxel in SKOV3-TR cells by inhibiting EGFR signaling and elevating intracellular ROS levels. Full article
(This article belongs to the Special Issue Anticancer Research: Towards an Understanding of Cancer and Discovery of New Therapeutic Agents)
►▼ Show Figures

Graphical abstract

16 pages, 7723 KiB  
Article
Elaiophylin Elicits Robust Anti-Tumor Responses via Apoptosis Induction and Attenuation of Proliferation, Migration, Invasion, and Angiogenesis in Pancreatic Cancer Cells
by Lufen Huang, Yufeng Liu, Yiru Pan, Chao Liu, Huijie Gao, Qiang Ren, Jianan Wang, Huiyun Wang, Yuntao Zhang and Anguo Wu
Molecules 2023, 28(20), 7205; https://doi.org/10.3390/molecules28207205 - 21 Oct 2023
Viewed by 947
Abstract
Pancreatic cancer remains a formidable challenge in oncology due to its aggressive nature and limited treatment options. In this study, we investigate the potential therapeutic efficacy of elaiophylin, a novel compound, in targeting BxPC-3 and PANC-1 pancreatic cancer cells. We comprehensively explore elaiophylin’s [...] Read more.
Pancreatic cancer remains a formidable challenge in oncology due to its aggressive nature and limited treatment options. In this study, we investigate the potential therapeutic efficacy of elaiophylin, a novel compound, in targeting BxPC-3 and PANC-1 pancreatic cancer cells. We comprehensively explore elaiophylin’s impact on apoptosis induction, proliferation inhibition, migration suppression, invasion attenuation, and angiogenesis inhibition, key processes contributing to cancer progression and metastasis. The results demonstrate that elaiophylin exerts potent pro-apoptotic effects, inducing a substantial increase in apoptotic cells. Additionally, elaiophylin significantly inhibits proliferation, migration, and invasion of BxPC-3 and PANC-1 cells. Furthermore, elaiophylin exhibits remarkable anti-angiogenic activity, effectively disrupting tube formation in HUVECs. Moreover, elaiophylin significantly inhibits the Wnt/β-Catenin signaling pathway. Our findings collectively demonstrate the multifaceted potential of elaiophylin as a promising therapeutic agent against pancreatic cancer via inhibition of the Wnt/β-Catenin signaling pathway. By targeting diverse cellular processes crucial for cancer progression, elaiophylin emerges as a prospective candidate for future targeted therapies. Further investigation of the in vivo efficacy of elaiophylin is warranted, potentially paving the way for novel and effective treatment approaches in pancreatic cancer management. Full article
(This article belongs to the Special Issue Anticancer Research: Towards an Understanding of Cancer and Discovery of New Therapeutic Agents)
►▼ Show Figures

Figure 1

13 pages, 3344 KiB  
Article
In Vitro Cytotoxic Effects and Mechanisms of Action of Eleutherine Isolated from Eleutherine plicata Bulb in Rat Glioma C6 Cells
by Victoria Mae Tsuruzaki Shinkai, Izana Marize Oliveira Sampaio, Eline Gomes dos Santos, Adan Jesús Galué-Parra, Dionisia Pelaes Ferreira, Drielly Dayanne Monteiro Santos Baliza, Neidiane Farias Ramos, Raphael Sanzio Pimenta, Rommel Mario Rodriguez Burbano, Chubert Bernardo Castro Sena, Barbarella Matos Macchi, Irlon Maciel Ferreira, Edilene Oliveira Silva and José Luiz Martins do Nascimento
Molecules 2022, 27(24), 8850; https://doi.org/10.3390/molecules27248850 - 13 Dec 2022
Cited by 2 | Viewed by 1551
Abstract
Gliomas are the most common primary malignant brain tumors in adults, and have a poor prognosis, despite the different types of treatment available. There is growing demand for new therapies to treat this life-threatening tumor. Quinone derivatives from plants have received increased interest [...] Read more.
Gliomas are the most common primary malignant brain tumors in adults, and have a poor prognosis, despite the different types of treatment available. There is growing demand for new therapies to treat this life-threatening tumor. Quinone derivatives from plants have received increased interest as potential anti-glioma drugs, due to their diverse pharmacologic activities, such as inhibiting cell growth, inflammation, tumor invasion, and promoting tumor regression. Previous studies have demonstrated the anti-glioma activity of Eleutherine plicata, which is related to three main naphthoquinone compounds—eleutherine, isoeleutherine, and eleutherol—but their mechanism of action remains elusive. Thus, the aim of this study was to investigate the mechanism of action of eleutherine on rat C6 glioma. In vitro cytotoxicity was evaluated by MTT assay; morphological changes were evaluated by phase-contrast microscopy. Apoptosis was determined by annexin V–FITC–propidium iodide staining, and antiproliferative effects were assessed by wound migration and colony formation assays. Protein kinase B (AKT/pAKT) expression was measured by western blot, and telomerase reverse transcriptase mRNA was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Eleutherine reduced C6 cell proliferation in a dose-dependent manner, suppressed migration and invasion, induced apoptosis, and reduced AKT phosphorylation and telomerase expression. In summary, our results suggest that eleutherine has potential clinical use in treating glioma. Full article
(This article belongs to the Special Issue Anticancer Research: Towards an Understanding of Cancer and Discovery of New Therapeutic Agents)
►▼ Show Figures

Graphical abstract

22 pages, 4820 KiB  
Article
131I-C19 Iodide Radioisotope and Synthetic I-C19 Compounds as K-Ras4B–PDE6δ Inhibitors: A Novel Approach against Colorectal Cancer—Biological Characterization, Biokinetics and Dosimetry
by Pedro Cruz-Nova, Blanca Ocampo-García, Dayan Andrea Carrión-Estrada, Paola Briseño-Diaz, Guillermina Ferro-Flores, Nallely Jiménez-Mancilla, José Correa-Basurto, Martiniano Bello, Libia Vega-Loyo, María del Rocío Thompson-Bonilla, Rosaura Hernández-Rivas and Miguel Vargas
Molecules 2022, 27(17), 5446; https://doi.org/10.3390/molecules27175446 - 25 Aug 2022
Cited by 3 | Viewed by 1738
Abstract
In 40–50% of colorectal cancer (CRC) cases, K-Ras gene mutations occur, which induce the expression of the K-Ras4B oncogenic isoform. K-Ras4B is transported by phosphodiesterase-6δ (PDE6δ) to the plasma membrane, where the K-Ras4B–PDE6δ complex dissociates and K-Ras4B, coupled to the plasma membrane, activates [...] Read more.
In 40–50% of colorectal cancer (CRC) cases, K-Ras gene mutations occur, which induce the expression of the K-Ras4B oncogenic isoform. K-Ras4B is transported by phosphodiesterase-6δ (PDE6δ) to the plasma membrane, where the K-Ras4B–PDE6δ complex dissociates and K-Ras4B, coupled to the plasma membrane, activates signaling pathways that favor cancer aggressiveness. Thus, the inhibition of the K-Ras4B–PDE6δ dissociation using specific small molecules could be a new strategy for the treatment of patients with CRC. This research aimed to perform a preclinical proof-of-concept and a therapeutic potential evaluation of the synthetic I-C19 and 131I-C19 compounds as inhibitors of the K-Ras4B–PDE6δ dissociation. Molecular docking and molecular dynamics simulations were performed to estimate the binding affinity and the anchorage sites of I-C19 in K-Ras4B–PDE6δ. K-Ras4B signaling pathways were assessed in HCT116, LoVo and SW620 colorectal cancer cells after I-C19 treatment. Two murine colorectal cancer models were used to evaluate the I-C19 therapeutic effect. The in vivo biokinetic profiles of I-C19 and 131I-C19 and the tumor radiation dose were also estimated. The K-Ras4B–PDE6δ stabilizer, 131I-C19, was highly selective and demonstrated a cytotoxic effect ten times greater than unlabeled I-C19. I-C19 prevented K-Ras4B activation and decreased its dependent signaling pathways. The in vivo administration of I-C19 (30 mg/kg) greatly reduced tumor growth in colorectal cancer. The biokinetic profile showed renal and hepatobiliary elimination, and the highest radiation absorbed dose was delivered to the tumor (52 Gy/74 MBq). The data support the idea that 131I-C19 is a novel K-Ras4B/PDE6δ stabilizer with two functionalities: as a K-Ras4B signaling inhibitor and as a compound with radiotherapeutic activity against colorectal tumors. Full article
(This article belongs to the Special Issue Anticancer Research: Towards an Understanding of Cancer and Discovery of New Therapeutic Agents)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop