Connection of Marine Natural Products and Cell Apoptosis—II

A special issue of Marine Drugs (ISSN 1660-3397).

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 3130

Special Issue Editors


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Guest Editor
Institute of Research, Development and Innovation in Healthcare Biotechnology of Elche (IDiBE), Miguel Hernández University (UMH), Alicante, Spain
Interests: natural compounds; polyphenols; marine compounds; cancer; antimicrobial; skin; cosmetics
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Instituto de Investigación, Desarrollo e Innovación en Biotecnologia Sanitaria at Miguel Hernández University, Elche, Spain
Interests: natural compounds; polyphenols; metabolic disorders; obesity; cancer; antimicrobial; skin; cosmetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The process of cell death is essential for the normal development and maintenance of the multicellularity of the organism. Programmed cell death is defined as the death of a cell in any physiopathological condition and refers to three main types: apoptosis, autophagy, and necroptosis. Although basal autophagy and apoptosis are essential for the maintenance of cellular and organism homeostasis, abnormal regulation of these processes contributes to the pathogenesis of various human diseases, including obesity, aging, and cancer. Thus, a better understanding of programmed cell death pathway alterations may lead to the identification of new drugs and to the development of new therapies against these abnormalities.

Marine natural products represent an almost unlimited source for the identification of novel molecules with anti-inflammatory, antihypertensive, and anti-tumorigenesis properties, possibly useful in the treatment or prevention of new anticancer drugs.

This Special Issue offers a review of our current understanding of the signaling pathways regulating cell death and highlights marine natural products that can affect these signaling pathways, with special interest in the “Connection of Marine Natural Products and Cell Apoptosis”. The putative molecular mechanisms of these extracts will be studied with special emphasis to metabolic alterations that contribute to the proliferation and aggressiveness of the tumor.

As Guest Editors, we cordially invite you to contribute to this Special Issue by submitting original research articles, long and mini review papers, short notes, and opinions according to your expertise.

Prof. Dr. María Herranz-López
Prof. Dr. Enrique Barrajon
Prof. Dr. Vicente Micol
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. Marine Drugs 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 2900 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

  • Apoptosis
  • Marine natural products
  • Cell biology
  • ROS
  • DNA damage
  • Mitochondrial depolarization
  • Autophagy
  • Cancer
  • Metabolic disorders

Published Papers (1 paper)

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Research

23 pages, 8011 KiB  
Article
13-Acetoxysarcocrassolide Exhibits Cytotoxic Activity against Oral Cancer Cells through the Interruption of the Keap1/Nrf2/p62/SQSTM1 Pathway: The Need to Move Beyond Classical Concepts
by Yi-Chang Liu, Bo-Rong Peng, Kai-Cheng Hsu, Mohamed El-Shazly, Shou-Ping Shih, Tony Eight Lin, Fu-Wen Kuo, Yi-Cheng Chou, Hung-Yu Lin and Mei-Chin Lu
Mar. Drugs 2020, 18(8), 382; https://doi.org/10.3390/md18080382 - 23 Jul 2020
Cited by 23 | Viewed by 2602
Abstract
13-Acetoxysarcocrassolide (13-AC), a marine cytotoxic product isolated from the alcyonacean coral Lobophytum crassum, exhibited potent antitumor and immunostimulant effects as reported in previous studies. However, the 13-AC antitumor mechanism of action against oral cancer cells remains unclear. The activity of 13-AC against [...] Read more.
13-Acetoxysarcocrassolide (13-AC), a marine cytotoxic product isolated from the alcyonacean coral Lobophytum crassum, exhibited potent antitumor and immunostimulant effects as reported in previous studies. However, the 13-AC antitumor mechanism of action against oral cancer cells remains unclear. The activity of 13-AC against Ca9-22 cancer cells was determined using MTT assay, flow cytometric analysis, immunofluorescence, immunoprecipitation, Western blotting, and siRNA. 13-AC induced apoptosis in oral cancer cells Ca9-22 through the disruption of mitochondrial membrane potential (MMP) and the stimulation of reactive oxygen species (ROS) generation. It increased the expression of apoptosis- and DNA damage-related proteins in a concentration- and time-dependent manner. It exerted potent antitumor effect against oral cancer cells, as demonstrated by the in vivo xenograft animal model. It significantly reduced the tumor volume (55.29%) and tumor weight (90.33%). The pretreatment of Ca9-22 cells with N-acetylcysteine (NAC) inhibited ROS production resulting in the attenuation of the cytotoxic activity of 13-AC. The induction of the Keap1-Nrf2 pathway and the promotion of p62/SQSTM1 were observed in Ca9-22 cells treated with 13-AC. The knockdown of p62 expression by siRNA transfection significantly attenuated the effect of 13-AC on the inhibition of cell viability. Our results indicate that 13-AC exerted its cytotoxic activity through the promotion of ROS generation and the suppression of the antioxidant enzyme activity. The apoptotic effect of 13-AC was found to be mediated through the interruption of the Keap1/Nrf2/p62/SQSTM1 pathway, suggesting its potential future application as an anticancer agent. Full article
(This article belongs to the Special Issue Connection of Marine Natural Products and Cell Apoptosis—II)
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