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Molecular Oncology–Unmask the True Nature of Cancer
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Molecular Oncology–Unmask the True Nature of Cancer

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (25 March 2021) | Viewed by 21122

Special Issue Editors

Dr. Keiko Kawauchi

E-Mail Website
Guest Editor
Faculty of Frontiers of Innovative Research in Science and Technology (FIRST), Konan University, Kobe 658-8501, Hyogo, Japan
Interests: tumor suppressor; oncogene; signal transduction; actin cytoskeleton; mechanosignal transduction
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Nobuyuki Tanaka

E-Mail Website
Guest Editor
Institute for Advanced Medical Sciences, Nippon Medical School, Bunkyo-ku, Tokio 113-8602, Japan
Interests: tumor suppressor; oncogene; cancer stem cells; signal transduction; apoptosis
Dr. Masashi Okada

E-Mail Website
Guest Editor
Department of Molecular Cancer Science, Yamagata University School of Medicine, Yamagata 990-9585, Japan
Interests: cancer stem cells; tumor initiation; drug repositioning; cancer energy metabolism

Special Issue Information

Dear Colleagues,

A growing body of basic research in the field of molecular oncology has allowed for prolonged prognosis through the development of molecular targeted drugs, therapies, and diagnostic technologies. However, the development of drugs and therapies with other strategies is needed to improve patient survival because the complete cure of various cancers is difficult using current therapies. We currently have an incomplete understanding of the true nature of cancer. To unmask it, multiple conditions must be considered and controlled. Not only gene mutations in cancer cells but also the chemical and the mechanical environments surrounding cancer cells influence cancer cell behaviors such as proliferation, invasion, metastasis, and response to treatments.

The purpose of this Special Issue is to publish original research papers and review articles describing the molecular mechanisms of cancer initiation, progression, and therapeutics. A particular focus will be given to papers discussing the molecular mechanisms of when, where, or how gene expression and subcellular structure changes in cancer cells or their surrounding cells, such as cancer-associated immune cells and the fibroblasts, modulate cancer cell behaviors. Furthermore, papers reporting cancer cell responses to drugs or therapeutic method development to cure cancer will also be considered.

Dr. Keiko Kawauchi
Prof. Nobuyuki Tanaka
Dr. Masashi Okada
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. Genes 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 2600 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

  • cancer
  • cancer stem cells
  • immune system
  • gene mutation
  • oncogene
  • tumor suppressor
  • metabolism
  • organelle
  • cytoskeleton
  • microenvironment
  • epigenetic regulation
  • gene expression
  • signal transduction mechanosignal transduction

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Published Papers (6 papers)

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Research

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21 pages, 5482 KiB  
Article
Krüppel-Like Factor 4 and Its Activator APTO-253 Induce NOXA-Mediated, p53-Independent Apoptosis in Triple-Negative Breast Cancer Cells
by Wataru Nakajima, Kai Miyazaki, Yumi Asano, Satoshi Kubota and Nobuyuki Tanaka
Genes 2021, 12(4), 539; https://doi.org/10.3390/genes12040539 - 8 Apr 2021
Cited by 13 | Viewed by 2600
Abstract
Inducing apoptosis is an effective treatment for cancer. Conventional cytotoxic anticancer agents induce apoptosis primarily through activation of tumor suppressor p53 by causing DNA damage and the resulting regulation of B-cell leukemia/lymphoma-2 (BCL-2) family proteins. Therefore, the effects of these agents are limited [...] Read more.
Inducing apoptosis is an effective treatment for cancer. Conventional cytotoxic anticancer agents induce apoptosis primarily through activation of tumor suppressor p53 by causing DNA damage and the resulting regulation of B-cell leukemia/lymphoma-2 (BCL-2) family proteins. Therefore, the effects of these agents are limited in cancers where p53 loss-of-function mutations are common, such as triple-negative breast cancer (TNBC). Here, we demonstrate that ultraviolet (UV) light-induced p53-independent transcriptional activation of NOXA, a proapoptotic factor in the BCL-2 family, results in apoptosis induction. This UV light-induced NOXA expression was triggered by extracellular signal-regulated kinase (ERK) activity. Moreover, we identified the specific UV light-inducible DNA element of the NOXA promoter and found that this sequence is responsible for transcription factor Krüppel-like factor 4 (KLF4)-mediated induction. In p53-mutated TNBC cells, inhibition of KLF4 by RNA interference reduced NOXA expression. Furthermore, treatment of TNBC cells with a KLF4-inducing small compound, APTO-253, resulted in the induction of NOXA expression and NOXA-mediated apoptosis. Therefore, our results help to clarify the molecular mechanism of DNA damage-induced apoptosis and provide support for a possible treatment method for p53-mutated cancers. Full article
(This article belongs to the Special Issue Molecular Oncology–Unmask the True Nature of Cancer)
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24 pages, 6761 KiB  
Article
Differential Expression of a Panel of Ten CNTN1-Associated Genes during Prostate Cancer Progression and the Predictive Properties of the Panel towards Prostate Cancer Relapse
by Yan Gu, Mathilda Jing Chow, Anil Kapoor, Xiaozeng Lin, Wenjuan Mei and Damu Tang
Genes 2021, 12(2), 257; https://doi.org/10.3390/genes12020257 - 10 Feb 2021
Cited by 4 | Viewed by 2797
Abstract
Contactin 1 (CNTN1) is a new oncogenic protein of prostate cancer (PC); its impact on PC remains incompletely understood. We observed CNTN1 upregulation in LNCaP cell-derived castration-resistant PCs (CRPC) and CNTN1-mediated enhancement of LNCaP cell proliferation. CNTN1 overexpression in LNCaP cells resulted in [...] Read more.
Contactin 1 (CNTN1) is a new oncogenic protein of prostate cancer (PC); its impact on PC remains incompletely understood. We observed CNTN1 upregulation in LNCaP cell-derived castration-resistant PCs (CRPC) and CNTN1-mediated enhancement of LNCaP cell proliferation. CNTN1 overexpression in LNCaP cells resulted in enrichment of the CREIGHTON_ENDOCRINE_THERAPY_RESISTANCE_3 gene set that facilitates endocrine resistance in breast cancer. The leading-edge (LE) genes (n = 10) of this enrichment consist of four genes with limited knowledge on PC and six genes novel to PC. These LE genes display differential expression during PC initiation, metastatic progression, and CRPC development, and they predict PC relapse following curative therapies at hazard ratio (HR) 2.72, 95% confidence interval (CI) 1.96–3.77, and p = 1.77 × 10−9 in The Cancer Genome Atlas (TCGA) PanCancer cohort (n = 492) and HR 2.72, 95% CI 1.84–4.01, and p = 4.99 × 10−7 in Memorial Sloan Kettering Cancer Center (MSKCC) cohort (n = 140). The LE gene panel classifies high-, moderate-, and low-risk of PC relapse in both cohorts. Additionally, the gene panel robustly predicts poor overall survival in clear cell renal cell carcinoma (ccRCC, p = 1.13 × 10−11), consistent with ccRCC and PC both being urogenital cancers. Collectively, we report multiple CNTN1-related genes relevant to PC and their biomarker values in predicting PC relapse. Full article
(This article belongs to the Special Issue Molecular Oncology–Unmask the True Nature of Cancer)
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13 pages, 6726 KiB  
Article
Inhibition of the Lipid Droplet–Peroxisome Proliferator-Activated Receptor α Axis Suppresses Cancer Stem Cell Properties
by Kenta Kuramoto, Masahiro Yamamoto, Shuhei Suzuki, Keita Togashi, Tomomi Sanomachi, Chifumi Kitanaka and Masashi Okada
Genes 2021, 12(1), 99; https://doi.org/10.3390/genes12010099 - 14 Jan 2021
Cited by 27 | Viewed by 3460
Abstract
Cancer stem cells (CSCs), having both self-renewal and tumorigenic capacity, utilize an energy metabolism system different from that of non-CSCs. Lipid droplets (LDs) are organelles that store neutral lipids, including triacylglycerol. Previous studies demonstrated that LDs are formed and store lipids as an [...] Read more.
Cancer stem cells (CSCs), having both self-renewal and tumorigenic capacity, utilize an energy metabolism system different from that of non-CSCs. Lipid droplets (LDs) are organelles that store neutral lipids, including triacylglycerol. Previous studies demonstrated that LDs are formed and store lipids as an energy source in some CSCs. LDs play central roles not only in lipid storage, but also as a source of endogenous lipid ligands, which are involved in numerous signaling pathways, including the peroxisome proliferator-activated receptor (PPAR) signaling pathway. However, it remains unclear whether LD-derived signal transduction is involved in the maintenance of the properties of CSCs. We investigated the roles of LDs in cancer stemness using pancreatic and colorectal CSCs and isogenic non-CSCs. PPARα was activated in CSCs in which LDs accumulated, but not in non-CSCs, and pharmacological and genetic inhibition of PPARα suppressed cancer stemness. In addition, inhibition of both re-esterification and lipolysis pathways suppressed cancer stemness. Our study suggested that LD metabolic turnover accompanying PPARα activation is a promising anti-CSC therapeutic target. Full article
(This article belongs to the Special Issue Molecular Oncology–Unmask the True Nature of Cancer)
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10 pages, 529 KiB  
Article
Total Tumor Load of mRNA Cytokeratin 19 in the Sentinel Lymph Node as a Predictive Value of Axillary Lymphadenectomy in Patients with Neoadjuvant Breast Cancer
by Karla B. Peña, Amillano Kepa, Alba Cochs, Francesc Riu, David Parada and Josep Gumà
Genes 2021, 12(1), 77; https://doi.org/10.3390/genes12010077 - 8 Jan 2021
Cited by 7 | Viewed by 2502
Abstract
Although sentinel lymph node biopsy (SLNB) has proved to be able to diagnose axillary lymph node status safely and reliably, there is still not enough evidence to suggest that it can be used in patients who have undergone neoadjuvant chemotherapy (NAC) for lymph [...] Read more.
Although sentinel lymph node biopsy (SLNB) has proved to be able to diagnose axillary lymph node status safely and reliably, there is still not enough evidence to suggest that it can be used in patients who have undergone neoadjuvant chemotherapy (NAC) for lymph node-sparing surgery. The present study used molecular approaches to determine whether SLNB can be reliably used in patients who have been treated with NAC before SLN surgery, and whether the total tumor load of the SLN can be used as a predictive factor in axillary lymphadenectomy (ALD). We used one-step nucleic acid amplification (OSNA) to analyze a total of 111 consecutive patients who presented operable invasive breast carcinomas and who had been treated with NAC. SLN was positive in 55 patients and the identification rate was 100%. In 9 of these 55 patients, ALD showed that other lymph nodes were also involved. In all of the other 46 patients, the only lymph node to be identified as positive was SLN. Metastasis was not found in any of the axillary lymph nodes in the isolated tumor cell group. The total tumor load, defined as the amount of cytokeratin 19 mRNA copy numbers in all positives SLN (copies/µL), showed three risk groups related to the possibility of positive non-sentinel nodes. OSNA is a diagnostic technique that is highly sensitive, specific, and reproducible and it can be used to analyze sentinel lymph nodes after NAC. Total tumor load may be able to help predict additional metastases in axillary lymphadenectomy. Full article
(This article belongs to the Special Issue Molecular Oncology–Unmask the True Nature of Cancer)
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Review

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12 pages, 9095 KiB  
Review
Challenges and Opportunities in NUT Carcinoma Research
by Bin Gu and Maxwell C. Hakun
Genes 2021, 12(2), 235; https://doi.org/10.3390/genes12020235 - 5 Feb 2021
Cited by 6 | Viewed by 4149
Abstract
NUT carcinoma (NC) is a type of aggressive cancer driven by chromosome translocations. Fusion genes between a DNA-binding protein, such as bromodomain and extraterminal domain (BET) proteins, and the testis-specific protein NUTM1 generated by these translocations drive the formation of NC. NC can [...] Read more.
NUT carcinoma (NC) is a type of aggressive cancer driven by chromosome translocations. Fusion genes between a DNA-binding protein, such as bromodomain and extraterminal domain (BET) proteins, and the testis-specific protein NUTM1 generated by these translocations drive the formation of NC. NC can develop in very young children without significant accumulation of somatic mutations, presenting a relatively clean model to study the genetic etiology of oncogenesis. However, after 20 years of research, a few challenging questions still remain for understanding the mechanism and developing therapeutics for NC. In this short review, we first briefly summarize the current knowledge regarding the molecular mechanism and targeted therapy development of NC. We then raise three challenging questions: (1) What is the cell of origin of NC? (2) How does the germline analogous epigenetic reprogramming process driven by the BET-NUTM1 fusion proteins cause NC? and (3) How will BET-NUTM1 targeted therapies be developed? We propose that with the unprecedented technological advancements in genome editing, animal models, stem cell biology, organoids, and chemical biology, we have unique opportunities to address these challenges. Full article
(This article belongs to the Special Issue Molecular Oncology–Unmask the True Nature of Cancer)
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13 pages, 1345 KiB  
Review
Photosensitizers Based on G-Quadruplex Ligand for Cancer Photodynamic Therapy
by Keiko Kawauchi, Ryoto Urano, Natsuki Kinoshita, Shin Kuwamoto, Takeru Torii, Yoshiki Hashimoto, Shinya Taniguchi, Mitsuki Tsuruta and Daisuke Miyoshi
Genes 2020, 11(11), 1340; https://doi.org/10.3390/genes11111340 - 12 Nov 2020
Cited by 25 | Viewed by 4685
Abstract
G-quadruplex (G4) is the non-canonical secondary structure of DNA and RNA formed by guanine-rich sequences. G4-forming sequences are abundantly located in telomeric regions and in the promoter and untranslated regions (UTR) of cancer-related genes, such as RAS and MYC. Extensive research has [...] Read more.
G-quadruplex (G4) is the non-canonical secondary structure of DNA and RNA formed by guanine-rich sequences. G4-forming sequences are abundantly located in telomeric regions and in the promoter and untranslated regions (UTR) of cancer-related genes, such as RAS and MYC. Extensive research has suggested that G4 is a potential molecular target for cancer therapy. Here, we reviewed G4 ligands as photosensitizers for cancer photodynamic therapy (PDT), which is a minimally invasive therapeutic approach. The photosensitizers, such as porphyrins, were found to be highly toxic against cancer cells via the generation of reactive oxidative species (ROS) upon photo-irradiation. Several porphyrin derivatives and analogs, such as phthalocyanines, which can generate ROS upon photo-irradiation, have been reported to act as G4 ligands. Therefore, they have been implicated as promising photosensitizers that can selectively break down cancer-related DNA and RNA forming G4. In this review, we majorly focused on the potential application of G4 ligands as photosensitizers, which would provide a novel strategy for PDT, especially molecularly targeted PDT (mtPDT). Full article
(This article belongs to the Special Issue Molecular Oncology–Unmask the True Nature of Cancer)
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