Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Clarification of Mechanism of Carcinogenesis
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Clarification of Mechanism of Carcinogenesis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 34613

Special Issue Editors

Dr. Takaaki Masuda

E-Mail Website
Guest Editor
Department of Surgery, Kyushu University Beppu Hospital, 4546 Tsurumihara, Beppu 8740838, Japan
Interests: intratumor heterogeneity (ITH); cancer specific transcriptomes; non-coding genes; genomic alterations
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Koshi Mimori

E-Mail Website
Guest Editor
Department of Surgery, Kyushu University Beppu Hospital, 4546 Tsurumihara, Beppu 8740838, Japan
Interests: cancer genomics; cancer evolution; tumor immune response; liquid biopsy; GI cancers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Carcinogenesis is a multiparametric process that involves various factors, such as genetic, epigenetic, immune system-based, and environmental factors. Understanding the fundamental and underlying mechanisms of carcinogenesis at the cellular and molecular levels is essential for developing new therapeutic strategies for malignancies.

Recent innovative scientific technology, such as gene targeting with the CRISPR Cas system and bioinformatic analysis, using next generation sequencing or artificial intelligence, has significantly contributed to our understanding of tumor biology. Besides, host immunity has been brought back into the spotlight in tumor progression. This Special Issue will focus on carcinogenesis and will gather novel works dealing with the mechanisms involved in carcinogenesis, by biological or bioinformatic analysis. Both original manuscripts and critical reviews are welcome.

Dr. Takaaki Masuda
Prof. Dr. Koshi Mimori
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • carcinogenesis
  • bioinformatics
  • mathematical modeling
  • gene targeting

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Related Special Issue

Published Papers (6 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

Jump to: Review

15 pages, 6212 KiB  
Article
RNA Exosome Component EXOSC4 Amplified in Multiple Cancer Types Is Required for the Cancer Cell Survival
by Kenzui Taniue, Tanzina Tanu, Yuki Shimoura, Shuhei Mitsutomi, Han Han, Rika Kakisaka, Yusuke Ono, Nobue Tamamura, Kenji Takahashi, Youichiro Wada, Yusuke Mizukami and Nobuyoshi Akimitsu
Int. J. Mol. Sci. 2022, 23(1), 496; https://doi.org/10.3390/ijms23010496 - 2 Jan 2022
Cited by 11 | Viewed by 3473
Abstract
The RNA exosome is a multi-subunit ribonuclease complex that is evolutionally conserved and the major cellular machinery for the surveillance, processing, degradation, and turnover of diverse RNAs essential for cell viability. Here we performed integrated genomic and clinicopathological analyses of 27 RNA exosome [...] Read more.
The RNA exosome is a multi-subunit ribonuclease complex that is evolutionally conserved and the major cellular machinery for the surveillance, processing, degradation, and turnover of diverse RNAs essential for cell viability. Here we performed integrated genomic and clinicopathological analyses of 27 RNA exosome components across 32 tumor types using The Cancer Genome Atlas PanCancer Atlas Studies’ datasets. We discovered that the EXOSC4 gene, which encodes a barrel component of the RNA exosome, was amplified across multiple cancer types. We further found that EXOSC4 alteration is associated with a poor prognosis of pancreatic cancer patients. Moreover, we demonstrated that EXOSC4 is required for the survival of pancreatic cancer cells. EXOSC4 also repressed BIK expression and destabilized SESN2 mRNA by promoting its degradation. Furthermore, knockdown of BIK and SESN2 could partially rescue pancreatic cells from the reduction in cell viability caused by EXOSC4 knockdown. Our study provides evidence for EXOSC4-mediated regulation of BIK and SESN2 mRNA in the survival of pancreatic tumor cells. Full article
(This article belongs to the Special Issue Clarification of Mechanism of Carcinogenesis)
►▼ Show Figures

Figure 1

12 pages, 1605 KiB  
Article
Effects of 1,2-Dimethylhydrazine on Barrier Properties of Rat Large Intestine and IPEC-J2 Cells
by Viktoria Bekusova, Linda Droessler, Salah Amasheh and Alexander G. Markov
Int. J. Mol. Sci. 2021, 22(19), 10278; https://doi.org/10.3390/ijms221910278 - 24 Sep 2021
Cited by 3 | Viewed by 2323
Abstract
Colon cancer is accompanied by a decrease of epithelial barrier properties, which are determined by tight junction (TJ) proteins between adjacent epithelial cells. The aim of the current study was to analyze the expression of TJ proteins in a rat model of 1,2-dimethylhydrazine [...] Read more.
Colon cancer is accompanied by a decrease of epithelial barrier properties, which are determined by tight junction (TJ) proteins between adjacent epithelial cells. The aim of the current study was to analyze the expression of TJ proteins in a rat model of 1,2-dimethylhydrazine (DMH)-induced colorectal cancer, as well as the barrier properties and TJ protein expression of IPEC-J2 cell monolayers after incubation with DMH. Transepithelial electrical resistance and paracellular permeability for sodium fluorescein of IPEC-J2 were examined by an epithelial volt/ohm meter and spectrophotometry. The expression and localization of TJ proteins were analyzed by immunoblotting and immunohistochemistry. In the colonic tumors of rats with DMH-induced carcinogenesis, the expression of claudin-3 and -4 was significantly increased compared to controls. The transepithelial electrical resistance of IPEC-J2 cells increased, while paracellular permeability for sodium fluorescein decreased, accompanied by an increased expression of claudin-4. The increase of claudin-4 in rat colon after chronic DMH exposure was consistent with the acute effect of DMH on IPEC-J2 cells, which may indicate an essential role of this protein in colorectal cancer development. Full article
(This article belongs to the Special Issue Clarification of Mechanism of Carcinogenesis)
►▼ Show Figures

Figure 1

17 pages, 17318 KiB  
Article
Characterization of the Survival Influential Genes in Carcinogenesis
by Divya Sahu, Yu-Lin Chang, Yin-Chen Lin and Chen-Ching Lin
Int. J. Mol. Sci. 2021, 22(9), 4384; https://doi.org/10.3390/ijms22094384 - 22 Apr 2021
Cited by 2 | Viewed by 2231
Abstract
The genes influencing cancer patient mortality have been studied by survival analysis for many years. However, most studies utilized them only to support their findings associated with patient prognosis: their roles in carcinogenesis have not yet been revealed. Herein, we applied an in [...] Read more.
The genes influencing cancer patient mortality have been studied by survival analysis for many years. However, most studies utilized them only to support their findings associated with patient prognosis: their roles in carcinogenesis have not yet been revealed. Herein, we applied an in silico approach, integrating the Cox regression model with effect size estimated by the Monte Carlo algorithm, to screen survival-influential genes in more than 6000 tumor samples across 16 cancer types. We observed that the survival-influential genes had cancer-dependent properties. Moreover, the functional modules formed by the harmful genes were consistently associated with cell cycle in 12 out of the 16 cancer types and pan-cancer, showing that dysregulation of the cell cycle could harm patient prognosis in cancer. The functional modules formed by the protective genes are more diverse in cancers; the most prevalent functions are relevant for immune response, implying that patients with different cancer types might develop different mechanisms against carcinogenesis. We also identified a harmful set of 10 genes, with potential as prognostic biomarkers in pan-cancer. Briefly, our results demonstrated that the survival-influential genes could reveal underlying mechanisms in carcinogenesis and might provide clues for developing therapeutic targets for cancers. Full article
(This article belongs to the Special Issue Clarification of Mechanism of Carcinogenesis)
►▼ Show Figures

Figure 1

Review

Jump to: Research

37 pages, 925 KiB  
Review
Inflammation-Induced Tumorigenesis and Metastasis
by Sana Hibino, Tetsuro Kawazoe, Hidenori Kasahara, Shinji Itoh, Takatsugu Ishimoto, Mamiko Sakata-Yanagimoto and Koji Taniguchi
Int. J. Mol. Sci. 2021, 22(11), 5421; https://doi.org/10.3390/ijms22115421 - 21 May 2021
Cited by 121 | Viewed by 15364
Abstract
Inflammation, especially chronic inflammation, plays a pivotal role in tumorigenesis and metastasis through various mechanisms and is now recognized as a hallmark of cancer and an attractive therapeutic target in cancer. In this review, we discuss recent advances in molecular mechanisms of how [...] Read more.
Inflammation, especially chronic inflammation, plays a pivotal role in tumorigenesis and metastasis through various mechanisms and is now recognized as a hallmark of cancer and an attractive therapeutic target in cancer. In this review, we discuss recent advances in molecular mechanisms of how inflammation promotes tumorigenesis and metastasis and suppresses anti-tumor immunity in various types of solid tumors, including esophageal, gastric, colorectal, liver, and pancreatic cancer as well as hematopoietic malignancies. Full article
(This article belongs to the Special Issue Clarification of Mechanism of Carcinogenesis)
►▼ Show Figures

Figure 1

22 pages, 1214 KiB  
Review
SRC-3, a Steroid Receptor Coactivator: Implication in Cancer
by Licen Li, Chu-Xia Deng and Qiang Chen
Int. J. Mol. Sci. 2021, 22(9), 4760; https://doi.org/10.3390/ijms22094760 - 30 Apr 2021
Cited by 18 | Viewed by 4597
Abstract
Steroid receptor coactivator-3 (SRC-3), also known as amplified in breast cancer 1 (AIB1), is a member of the SRC family. SRC-3 regulates not only the transcriptional activity of nuclear receptors but also many other transcription factors. Besides the essential role of SRC-3 in [...] Read more.
Steroid receptor coactivator-3 (SRC-3), also known as amplified in breast cancer 1 (AIB1), is a member of the SRC family. SRC-3 regulates not only the transcriptional activity of nuclear receptors but also many other transcription factors. Besides the essential role of SRC-3 in physiological functions, it also acts as an oncogene to promote multiple aspects of cancer. This review updates the important progress of SRC-3 in carcinogenesis and summarizes its mode of action, which provides clues for cancer therapy. Full article
(This article belongs to the Special Issue Clarification of Mechanism of Carcinogenesis)
►▼ Show Figures

Figure 1

15 pages, 1431 KiB  
Review
Mechanisms of High-Grade Serous Carcinogenesis in the Fallopian Tube and Ovary: Current Hypotheses, Etiologic Factors, and Molecular Alterations
by Isao Otsuka
Int. J. Mol. Sci. 2021, 22(9), 4409; https://doi.org/10.3390/ijms22094409 - 23 Apr 2021
Cited by 16 | Viewed by 5733
Abstract
Ovarian high-grade serous carcinomas (HGSCs) are a heterogeneous group of diseases. They include fallopian-tube-epithelium (FTE)-derived and ovarian-surface-epithelium (OSE)-derived tumors. The risk/protective factors suggest that the etiology of HGSCs is multifactorial. Inflammation caused by ovulation and retrograde bleeding may play a major role. HGSCs [...] Read more.
Ovarian high-grade serous carcinomas (HGSCs) are a heterogeneous group of diseases. They include fallopian-tube-epithelium (FTE)-derived and ovarian-surface-epithelium (OSE)-derived tumors. The risk/protective factors suggest that the etiology of HGSCs is multifactorial. Inflammation caused by ovulation and retrograde bleeding may play a major role. HGSCs are among the most genetically altered cancers, and TP53 mutations are ubiquitous. Key driving events other than TP53 mutations include homologous recombination (HR) deficiency, such as BRCA 1/2 dysfunction, and activation of the CCNE1 pathway. HR deficiency and the CCNE1 amplification appear to be mutually exclusive. Intratumor heterogeneity resulting from genomic instability can be observed at the early stage of tumorigenesis. In this review, I discuss current carcinogenic hypotheses, sites of origin, etiologic factors, and molecular alterations of HGSCs. Full article
(This article belongs to the Special Issue Clarification of Mechanism of Carcinogenesis)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-6
Back to TopTop