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Molecular Mechanism of Gastric Cancer

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: 31 July 2024 | Viewed by 2345

Special Issue Editor


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Guest Editor
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan 250012, China
Interests: the role of non-resolving inflammation on gastric carcinogenesis; the mechanism of invasion and metastasis of gastric carcinoma; the key markers for early diagnosis and treatment of gastric cancer

Special Issue Information

Dear Colleagues,

Gastric cancer is a major threat to the survival outcome of patients. Both the lack of effective early diagnosis and patients’ resistance to existing treatments result in poor prognosis. Therefore, revealing the malignant transformation mechanism implicated in gastric mucosa is essential to the early prevention and control of gastric cancer. Helicobacter pylori is an important factor causing gastric carcinogenesis, and has been identified as a Class I carcinogen by WHO/IARC. Microorganisms, with their residues and metabolites, can accumulate in and interact with cancer cells and immune cells to form the Tumor Microbial Microenvironment, which can induce the dysregulation of gene expression and cell proliferation via a variety of regulatory mechanisms. Meanwhile, gastric carcinoma cells in the TME can interact with innate immune cells, tumor-related fibroblasts, endothelial cells, pericytes and other non-tumor cells through cytokines to co-evolve and promote gastric carcinogenesis. It is essential to explore the mechanisms implicated in the transformation of malignant gastric mucosa and to detect the novel node molecules and regulatory targets involved in it; this is of great significance for the early diagnosis and treatment of gastric cancer.

Prof. Dr. Jiping Zeng
Guest Editor

Manuscript Submission Information

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Keywords

  • gastric cancer
  • Helicobacter pylori
  • cell death
  • cancer metabolism
  • tumor microenvironment
  • immunity and inflammation
  • epigenetics
  • non-coding RNAs
  • protein modification
  • bioinformatics

Published Papers (2 papers)

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Research

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17 pages, 4357 KiB  
Article
Pterostilbene Induces Apoptosis from Endoplasmic Reticulum Stress Synergistically with Anticancer Drugs That Deposit Iron in Mitochondria
by Yukiko Nishiguch, Rina Fujiwara-Tani, Shota Nukaga, Ryoichi Nishida, Ayaka Ikemoto, Rika Sasaki, Shiori Mori, Ruiko Ogata, Shingo Kishi, Yudai Hojo, Hisashi Shinohara, Masayuki Sho and Hiroki Kuniyasu
Int. J. Mol. Sci. 2024, 25(5), 2611; https://doi.org/10.3390/ijms25052611 - 23 Feb 2024
Cited by 1 | Viewed by 837
Abstract
Anticancer agents are playing an increasing role in the treatment of gastric cancer (GC); however, novel anticancer agents have not been fully developed. Therefore, it is important to investigate compounds that improve sensitivity to the existing anticancer drugs. We have reported that pterostilbene [...] Read more.
Anticancer agents are playing an increasing role in the treatment of gastric cancer (GC); however, novel anticancer agents have not been fully developed. Therefore, it is important to investigate compounds that improve sensitivity to the existing anticancer drugs. We have reported that pterostilbene (PTE), a plant stilbene, enhances the antitumor effect of low doses of sunitinib in gastric cancer cells accumulating mitochondrial iron (II) (mtFe) at low doses. In this study, we investigated the relationship between the mtFe deposition and the synergistic effect of PTE and different anticancer drugs. For this study, we used 5-fluorouracil (5FU), cisplatin (CPPD), and lapatinib (LAP), which are frequently used in the treatment of GC, and doxorubicin (DOX), which is known to deposit mtFe. A combination of low-dose PTE and these drugs suppressed the expression of PDZ domain-containing 8 (PDZD8) and increased mtFe accumulation and mitochondrial H2O2. Consequently, reactive oxygen species-associated hypoxia inducible factor-1α activation induced endoplasmic reticulum stress and led to apoptosis, but not ferroptosis. In contrast, 5FU and CDDP did not show the same changes as those observed with PTE and DOX or LAP, and there was no synergistic effect with PTE. These results indicate that the combination of PTE with iron-accumulating anticancer drugs exhibits a strong synergistic effect. These findings would help in developing novel therapeutic strategies for GC. However, further clinical investigations are required. Full article
(This article belongs to the Special Issue Molecular Mechanism of Gastric Cancer)
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Review

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30 pages, 5116 KiB  
Review
Molecular Classifications in Gastric Cancer: A Call for Interdisciplinary Collaboration
by Cristina Díaz del Arco, María Jesús Fernández Aceñero and Luis Ortega Medina
Int. J. Mol. Sci. 2024, 25(5), 2649; https://doi.org/10.3390/ijms25052649 - 24 Feb 2024
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Abstract
Gastric cancer (GC) is a heterogeneous disease, often diagnosed at advanced stages, with a 5-year survival rate of approximately 20%. Despite notable technological advancements in cancer research over the past decades, their impact on GC management and outcomes has been limited. Numerous molecular [...] Read more.
Gastric cancer (GC) is a heterogeneous disease, often diagnosed at advanced stages, with a 5-year survival rate of approximately 20%. Despite notable technological advancements in cancer research over the past decades, their impact on GC management and outcomes has been limited. Numerous molecular alterations have been identified in GC, leading to various molecular classifications, such as those developed by The Cancer Genome Atlas (TCGA) and the Asian Cancer Research Group (ACRG). Other authors have proposed alternative perspectives, including immune, proteomic, or epigenetic-based classifications. However, molecular stratification has not yet transitioned into clinical practice for GC, and little attention has been paid to alternative molecular classifications. In this review, we explore diverse molecular classifications in GC from a practical point of view, emphasizing their relationships with clinicopathological factors, prognosis, and therapeutic approaches. We have focused on classifications beyond those of TCGA and the ACRG, which have been less extensively reviewed previously. Additionally, we discuss the challenges that must be overcome to ensure their impact on patient treatment and prognosis. This review aims to serve as a practical framework to understand the molecular landscape of GC, facilitate the development of consensus molecular categories, and guide the design of innovative molecular studies in the field. Full article
(This article belongs to the Special Issue Molecular Mechanism of Gastric Cancer)
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