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Cells
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20th Anniversary of Nobel Prize 2002: Gene Regulation in Programmed...
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20th Anniversary of Nobel Prize 2002: Gene Regulation in Programmed Cell Death

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (15 March 2023) | Viewed by 14249

Special Issue Editors

Dr. Suchismita Raha

E-Mail Website
Guest Editor
1. Department of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Republic of Korea
2. Institute of Molecular Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA
Interests: tumor microenvironment; anti-cancer targets; cell signaling; cancer; programmed cell death; apoptosis; autophagy; lysosomal death; mitochondrial dysfunction; inflammatory disorder; protein-protein network; biomarker
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Gon Sup Kim

E-Mail Website
Guest Editor
Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Republic of Korea
Interests: bioactive therapeutics; monomer drug research; anti-cancer drug treatment; apoptosis; cell signaling pathways; anti-inflammatory disease drug treatment; protein biomarker
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The Nobel Prize in Physiology or Medicine 2002 was awarded to Sydney Brenner, Howard Robert Horvitz and John Edward Sulston for their seminal discoveries concerning “genetic regulation of organ development and programmed cell death”.

The Laureates used the nematode Caenorhabditis elegans as an experimental model system, which opened the possibility to follow cell division and differentiation from the fertilized egg to the adult and identify the key genes which regulate organ development and programmed cell death (PCD), a process used to eliminate excess cells.

In early 1960s, Sydney Brenner focused on C. elegans as a model organism of multicellular organisms that are simpler than mammals to carry out an investigation on cell differentiation and organ development for genetic analysis.

John E. Sulston mapped the cell lineage in C. elegans for the development of nervous system. This led to the groundbreaking discovery of PCD, which specifies that certain cells in the cell lineage are always destined to die; Sulston also demonstrated the first mutations of genes that participate in PCD.

H. Robert Horvitz identified the first two “death genes” in C. elegans, named ced-3 and ced-4; the prerequisite for cell death and ced-9 gene protects against cell death and showed that humans have a gene similar to one of these.

This seminal discovery led to a potential hallmark in developmental biology, which unfolded the core machinery behind the mechanisms of cell death. Over the decades, scientists have aimed to understand the regulatory forms of different PCDs and their underlying signaling network in the pathogenesis of many diseases such as cancer, neurodegeneration, developmental and inherited disorders, inflammatory diseases and during microbial infections and in aging. In the last 20 years, many new investigations have shed light on PCD-targeted therapy in order to find better treatment approaches.

This Special Issue of Cells welcomes submissions of original research articles and reviews covering unexpected findings and comprehensive approaches in the field of programmed cell death, as well as its implication in therapeutic targets and developmental process.

Dr. Suchismita Raha
Dr. Gon Sup Kim
Guest Editors

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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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • programmed cell death
  • programmed cell death in cell development
  • programmed cell death in disease and genetic disorder
  • programmed cell death in therapeutic targets
  • signaling and regulatory network
  • apoptosis cell death
  • autophagy cell death
  • necroptosis cell death
  • ferroptosis cell death

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Published Papers (4 papers)

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Research

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15 pages, 3756 KiB  
Article
Fabricated AIE-Based Probe to Detect the Resistance to Anoikis of Cancer Cells Detached from Tumor Tissue
by Ya-Nan Chang, Yuelan Liang, Jiayi Wang, Ziteng Chen, Ruyu Yan, Kui Chen, Juan Li, Jiacheng Li, Haojun Liang and Gengmei Xing
Cells 2022, 11(21), 3478; https://doi.org/10.3390/cells11213478 - 3 Nov 2022
Viewed by 1874
Abstract
(1) Background: Resisting anoikis is a vital and necessary characteristic of malignant cancer cells, but there is no existing quantification method. Herein, a sensitive probe for assessing anoikis resistance of cancer cells detached from the extracellular matrix was developed based on the aggregation-induced [...] Read more.
(1) Background: Resisting anoikis is a vital and necessary characteristic of malignant cancer cells, but there is no existing quantification method. Herein, a sensitive probe for assessing anoikis resistance of cancer cells detached from the extracellular matrix was developed based on the aggregation-induced emission (AIE) of AIEgens. It has been reported that detached cancer cell endocytose activated integrin clusters, and in the endosome these clusters recruit and activate phosphorylate focal adhesion kinase (pFAK) in the cytoplasm to induce signaling that supports the growth of detached cancer cells. (2) Methods: We established a lost nest cell model of cancer cells and determined their ability to resist anoikis. The colocalization of the activated integrin, pFAK, and endosomes in model cells was observed and calculated. (3) Results: The fluorescence signal intensity of the probe was significantly higher than that of the integrin antibody in the model cells and the fluorescence signal of probe signal was better overlapped with labeled pFAK by fluorescence in endosomes in model cells. (4) Conclusions: We developed a quantitative multi-parametric image analysis program to calculate fluorescent intensity of the probe and antibodies against pFAK and Rab5 in the areas of colocalization. A positive correlation of fluorescence signal intensity between the probe and pFAK on the endosome was observed. Therefore, the probe was used to quantitatively evaluate resisting anoikis of different cancer cell lines under the lost nest condition. Full article
(This article belongs to the Special Issue 20th Anniversary of Nobel Prize 2002: Gene Regulation in Programmed Cell Death)
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26 pages, 10759 KiB  
Article
Cuprotosis Programmed-Cell-Death-Related lncRNA Signature Predicts Prognosis and Immune Landscape in PAAD Patients
by Hao Chi, Gaoge Peng, Rui Wang, Fengyi Yang, Xixi Xie, Jinhao Zhang, Ke Xu, Tao Gu, Xiaoli Yang and Gang Tian
Cells 2022, 11(21), 3436; https://doi.org/10.3390/cells11213436 - 31 Oct 2022
Cited by 48 | Viewed by 2990
Abstract
In terms of mortality and survival, pancreatic cancer is one of the worst malignancies. Known as a unique type of programmed cell death, cuprotosis contributes to tumor cell growth, angiogenesis, and metastasis. Cuprotosis programmed-cell-death-related lncRNAs (CRLs) have been linked to PAAD, although their [...] Read more.
In terms of mortality and survival, pancreatic cancer is one of the worst malignancies. Known as a unique type of programmed cell death, cuprotosis contributes to tumor cell growth, angiogenesis, and metastasis. Cuprotosis programmed-cell-death-related lncRNAs (CRLs) have been linked to PAAD, although their functions in the tumor microenvironment and prognosis are not well understood. This study included data from the TCGA-PAAD cohort. Random sampling of PAAD data was conducted, splitting the data into two groups for use as a training set and test set (7:3). We searched for differentially expressed genes that were substantially linked to prognosis using univariate Cox and Lasso regression analysis. Through the use of multivariate Cox proportional risk regression, a risk-rating system for prognosis was developed. Correlations between the CRL signature and clinicopathological characteristics, tumor microenvironment, immunotherapy response, and chemotherapy sensitivity were further evaluated. Lastly, qRT-PCR was used to compare CRL expression in healthy tissues to that in tumors. Some CRLs are thought to have strong correlations with PAAD outcomes. These CRLs include AC005332.6, LINC02041, LINC00857, and AL117382.1. The CRL-based signature construction exhibited outstanding predictive performance and offers a fresh approach to evaluating pre-immune effectiveness, paving the way for future studies in precision immuno-oncology. Full article
(This article belongs to the Special Issue 20th Anniversary of Nobel Prize 2002: Gene Regulation in Programmed Cell Death)
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13 pages, 4023 KiB  
Article
Apigetrin Promotes TNFα-Induced Apoptosis, Necroptosis, G2/M Phase Cell Cycle Arrest, and ROS Generation through Inhibition of NF-κB Pathway in Hep3B Liver Cancer Cells
by Pritam Bhagwan Bhosale, Abuyaseer Abusaliya, Hun Hwan Kim, Sang Eun Ha, Min Yeong Park, Se Hyo Jeong, Preethi Vetrivel, Jeong Doo Heo, Jin-A Kim, Chung kil Won, Hyun-Wook Kim and Gon Sup Kim
Cells 2022, 11(17), 2734; https://doi.org/10.3390/cells11172734 - 1 Sep 2022
Cited by 24 | Viewed by 3653
Abstract
Apigetrin (7-(β-D-glucopyranosyloxy)-4′,5-dihydroxyflavone), a glycoside bioactive dietary flavonoid derived from Taraxacum officinale and Teucrium gnaphalodes, is known to possess anticancer, antioxidant, and anti-inflammatory effects on numerous cancers. In the present study, we examined the effect of apigetrin in Hep3B hepatocellular cancer cell line (HCC). [...] Read more.
Apigetrin (7-(β-D-glucopyranosyloxy)-4′,5-dihydroxyflavone), a glycoside bioactive dietary flavonoid derived from Taraxacum officinale and Teucrium gnaphalodes, is known to possess anticancer, antioxidant, and anti-inflammatory effects on numerous cancers. In the present study, we examined the effect of apigetrin in Hep3B hepatocellular cancer cell line (HCC). Apigetrin inhibited cell growth and proliferation of Hep3B cells, as confirmed by MTT and colony formation assay. We used apigetrin at concentrations of 0, 50, and 100 µM for later experiments. Of these concentrations, 100 µM of apigetrin showed a significant effect on cell inhibition. In apigetrin-treated Hep3B cells, cell cycle arrest occurred at the G2/M phase. Apoptosis and necroptosis of Hep3B cells treated with apigetrin were confirmed by Annexin V/propidium iodide (PI) staining and flow cytometry results. Morphological observation through 4′,6-diamidino-2-phenylindole (DAPI) staining showed intense blue fluorescence representing chromatin condensation. Hematoxylin staining showed necroptotic features such as formation of vacuoles and swelling of organelles. Apigetrin increased reactive oxygen species (ROS) levels in cells, based on fluorescence imaging. Furthermore, the underlying mechanism involved in the apoptosis and necroptosis was elucidated through western blotting. Apigetrin up-regulated TNFα, but down-regulated phosphorylation of p-p65, and IκB. Apigetrin inhibited the expression of Bcl-xl but increased Bax levels. Up-regulation of cleaved PARP and cleaved caspase 3 confirmed the induction of apoptosis in apigetrin-treated Hep3B cells. Additionally, necroptosis markers RIP3, p-RIP3, and p-MLKL were significantly elevated by apigetrin dose-dependently, suggesting necroptotic cell death. Taken together, our findings strongly imply that apigetrin can induce apoptosis and necroptosis of Hep3B hepatocellular cancer cells. Thus, apigetrin as a natural compound might have potential for treating liver cancer. Full article
(This article belongs to the Special Issue 20th Anniversary of Nobel Prize 2002: Gene Regulation in Programmed Cell Death)
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Review

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37 pages, 2465 KiB  
Review
Targeting TRAIL Death Receptors in Triple-Negative Breast Cancers: Challenges and Strategies for Cancer Therapy
by Manjari Kundu, Yoshimi Endo Greer, Jennifer L. Dine and Stanley Lipkowitz
Cells 2022, 11(23), 3717; https://doi.org/10.3390/cells11233717 - 22 Nov 2022
Cited by 9 | Viewed by 4456
Abstract
The tumor necrosis factor (TNF) superfamily member TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis in cancer cells via death receptor (DR) activation with little toxicity to normal cells or tissues. The selectivity for activating apoptosis in cancer cells confers an ideal therapeutic characteristic to [...] Read more.
The tumor necrosis factor (TNF) superfamily member TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis in cancer cells via death receptor (DR) activation with little toxicity to normal cells or tissues. The selectivity for activating apoptosis in cancer cells confers an ideal therapeutic characteristic to TRAIL, which has led to the development and clinical testing of many DR agonists. However, TRAIL/DR targeting therapies have been widely ineffective in clinical trials of various malignancies for reasons that remain poorly understood. Triple negative breast cancer (TNBC) has the worst prognosis among breast cancers. Targeting the TRAIL DR pathway has shown notable efficacy in a subset of TNBC in preclinical models but again has not shown appreciable activity in clinical trials. In this review, we will discuss the signaling components and mechanisms governing TRAIL pathway activation and clinical trial findings discussed with a focus on TNBC. Challenges and potential solutions for using DR agonists in the clinic are also discussed, including consideration of the pharmacokinetic and pharmacodynamic properties of DR agonists, patient selection by predictive biomarkers, and potential combination therapies. Moreover, recent findings on the impact of TRAIL treatment on the immune response, as well as novel strategies to address those challenges, are discussed. Full article
(This article belongs to the Special Issue 20th Anniversary of Nobel Prize 2002: Gene Regulation in Programmed Cell Death)
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