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Molecular Mechanism of Gastric Cancer
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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: closed (31 July 2024) | Viewed by 6312

Special Issue Editor

Prof. Dr. Jiping Zeng

E-Mail Website
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

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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

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Published Papers (4 papers)

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Research

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20 pages, 5807 KiB  
Article
ICAM1 (CD54) Contributes to the Metastatic Capacity of Gastric Cancer Stem Cells
by José Manuel Tinajero-Rodríguez, Lizbeth Ramírez-Vidal, Jared Becerril-Rico, Eduardo Alvarado-Ortiz, Dámaris P. Romero-Rodríguez, Fernando López-Casillas, Daniel Hernández-Sotelo, Fernando Fernández-Ramírez, Adriana Contreras-Paredes and Elizabeth Ortiz-Sánchez
Int. J. Mol. Sci. 2024, 25(16), 8865; https://doi.org/10.3390/ijms25168865 - 14 Aug 2024
Viewed by 559
Abstract
Gastric cancer is the fourth leading cause of cancer deaths worldwide. The presence of chemoresistant cells has been used to explain this high mortality rate. These higher tumorigenic and chemoresistant cells involve cancer stem cells (CSCs), which have the potential for self-renewal, a [...] Read more.
Gastric cancer is the fourth leading cause of cancer deaths worldwide. The presence of chemoresistant cells has been used to explain this high mortality rate. These higher tumorigenic and chemoresistant cells involve cancer stem cells (CSCs), which have the potential for self-renewal, a cell differentiation capacity, and a greater tumorigenic capacity. Our research group identified gastric cancer stem cells (GCSCs) with the CD24+CD44+CD326+ICAM1+ immunophenotype isolated from gastric cancer patients. Interestingly, this GCSC immunophenotype was absent in cells isolated from healthy people, who presented a cell population with a CD24+CD44+CD326+ immunophenotype, lacking ICAM1. We aimed to explore the role of ICAM1 in these GCSCs; for this purpose, we isolated GCSCs from the AGS cell line and generated a GCSC line knockout for ICAM1 using CRISPR/iCas9, which we named GCSC-ICAM1KO. To assess the role of ICAM1 in the GCSCs, we analyzed the migration, invasion, and chemoresistance capabilities of the GCSCs using in vitro assays and evaluated the migratory, invasive, and tumorigenic properties in a zebrafish model. The in vitro analysis showed that ICAM1 regulated STAT3 activation (pSTAT3-ser727) in the GCSCs, which could contribute to the ability of GCSCs to migrate, invade, and metastasize. Interestingly, we demonstrated that the GCSC-ICAM1KO cells lost their capacity to migrate, invade, and metastasize, but they exhibited an increased resistance to a cisplatin treatment compared to their parental GCSCs; the GCSC-ICAM1KO cells also exhibited an increased tumorigenic capability in vivo. Full article
(This article belongs to the Special Issue Molecular Mechanism of Gastric Cancer)
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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 2 | Viewed by 1456
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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17 pages, 694 KiB  
Review
The Impact of Tobacco Smoking and Alcohol Consumption on the Development of Gastric Cancers
by Waku Hatta, Tomoyuki Koike, Naoki Asano, Yutaka Hatayama, Yohei Ogata, Masahiro Saito, Xiaoyi Jin, Kaname Uno, Akira Imatani and Atsushi Masamune
Int. J. Mol. Sci. 2024, 25(14), 7854; https://doi.org/10.3390/ijms25147854 - 18 Jul 2024
Viewed by 1155
Abstract
Chronic infection of Helicobacter pylori is considered the principal cause of gastric cancers, but evidence has accumulated regarding the impact of tobacco smoking and alcohol consumption on the development of gastric cancers. Several possible mechanisms, including the activation of nicotinic acetylcholine receptors, have [...] Read more.
Chronic infection of Helicobacter pylori is considered the principal cause of gastric cancers, but evidence has accumulated regarding the impact of tobacco smoking and alcohol consumption on the development of gastric cancers. Several possible mechanisms, including the activation of nicotinic acetylcholine receptors, have been proposed for smoking-induced gastric carcinogenesis. On the other hand, local acetaldehyde exposure and ethanol-induced mucosal inflammation have been proposed as the mechanisms involved in the development of gastric cancers in heavy alcohol drinkers. In addition, genetic polymorphisms are also considered to play a pivotal role in smoking-related and alcohol-related gastric carcinogenesis. In this review, we will discuss the molecular mechanisms involved in the development of gastric cancers in relation to tobacco smoking and alcohol consumption. Full article
(This article belongs to the Special Issue Molecular Mechanism of Gastric Cancer)
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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
Cited by 4 | Viewed by 2629
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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