Inflammatory Cytokines Pathways as Potential Therapeutic Targets for Gastric Cancer

Despite mounting evidence demonstrating the significance of inflammation in the pathophysiological mechanisms of heart failure (HF), most large clinical trials that target the inflammatory responses in HF yielded neutral or even worsening outcomes. Further in-depth understanding about the roles of inflammation in the pathogenesis of HF is eagerly needed. This review summarizes cytokines, cardiac infiltrating immune cells, and extracardiac organs that orchestrate the complex inflammatory responses in HF and highlights emerging therapeutic targets.

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Mechanisms of Action And Clinical Implications of MicroRNAs in the Drug Resistance of Gastric Cancer

Frontiers in Oncology ◽

10.3389/fonc.2021.768918 ◽

2021 ◽

Vol 11 ◽

Author(s):

Ying Liu ◽

Xiang Ao ◽

Guoqiang Ji ◽

Yuan Zhang ◽

Wanpeng Yu ◽

...

Keyword(s):

Gastric Cancer ◽

Drug Resistance ◽

Molecular Mechanisms ◽

Malignant Tumors ◽

Life Quality ◽

Therapeutic Targets ◽

Chemotherapeutic Agents ◽

Response To Chemotherapy ◽

Novel Biomarkers ◽

Related Proteins

Gastric cancer (GC) is one of the most common malignant tumors of digestive systems worldwide, with high recurrence and mortality. Chemotherapy is still the standard treatment option for GC and can effectively improve the survival and life quality of GC patients. However, with the emergence of drug resistance, the clinical application of chemotherapeutic agents has been seriously restricted in GC patients. Although the mechanisms of drug resistance have been broadly investigated, they are still largely unknown. MicroRNAs (miRNAs) are a large group of small non-coding RNAs (ncRNAs) widely involved in the occurrence and progression of many cancer types, including GC. An increasing amount of evidence suggests that miRNAs may play crucial roles in the development of drug resistance by regulating some drug resistance-related proteins as well as gene expression. Some also exhibit great potential as novel biomarkers for predicting drug response to chemotherapy and therapeutic targets for GC patients. In this review, we systematically summarize recent advances in miRNAs and focus on their molecular mechanisms in the development of drug resistance in GC progression. We also highlight the potential of drug resistance-related miRNAs as biomarkers and therapeutic targets for GC patients.

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Long noncoding RNA FAM225A promotes the malignant progression of gastric cancer through the miR-326/PADI2 axis

Cell Death Discovery ◽

10.1038/s41420-021-00809-1 ◽

2022 ◽

Vol 8 (1) ◽

Author(s):

Xiang Ma ◽

Gang Wang ◽

Hao Fan ◽

Zengliang Li ◽

Wangwang Chen ◽

...

Keyword(s):

Gastric Cancer ◽

Noncoding Rna ◽

Molecular Mechanisms ◽

Therapeutic Targets ◽

In Vitro Assays ◽

Advanced Tumor Stage ◽

Advanced Tumor ◽

Mechanistic Investigation

AbstractGastric cancer (GC) is a global health problem and further studies of its molecular mechanisms are needed to identify effective therapeutic targets. Although some long noncoding RNAs (lncRNAs) have been found to be involved in the progression of GC, the molecular mechanisms of many GC-related lncRNAs remain unclear. In this study, a series of in vivo and in vitro assays were performed to study the relationship between FAM225A and GC, which showed that FAM225A levels were correlated with poor prognosis in GC. Higher FAM225A expression tended to be correlated with a more profound lymphatic metastasis rate, larger tumor size, and more advanced tumor stage. FAM225A also promoted gastric cell proliferation, invasion, and migration. Further mechanistic investigation showed that FAM225A acted as a miR-326 sponge to upregulate its direct target PADI2 in GC. Overall, our findings indicated that FAM225A promoted GC development and progression via a competitive endogenous RNA network of FAM225A/miR-326/PADI2 in GC, providing insight into possible therapeutic targets and prognosis of GC.

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Therapeutic targets against gastric cancer stem cells interacting with tumor microenvironment

Journal of Cancer Metastasis and Treatment ◽

10.20517/2394-4722.2017.81 ◽

2018 ◽

Vol 4 (2) ◽

pp. 9 ◽

Cited By ~ 1

Author(s):

Tomoyuki Uchihara ◽

Takatsugu Ishimoto ◽

Atsuko Yonemura ◽

Hideo Baba

Keyword(s):

Gastric Cancer ◽

Stem Cells ◽

Tumor Microenvironment ◽

Cancer Stem Cells ◽

Therapeutic Targets ◽

Gastric Cancer Stem Cells

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LINC01133 hampers the development of gastric cancer through increasing SST via binding to microRNA-576-5p

Epigenomics ◽

10.2217/epi-2020-0377 ◽

2021 ◽

Author(s):

Leiyi Zhang ◽

Ke Pan ◽

Zhongkun Zuo ◽

Fei Ye ◽

Ding Cao ◽

...

Keyword(s):

Gastric Cancer ◽

Tumor Growth ◽

Nude Mice ◽

Therapeutic Targets ◽

Loss Of Function ◽

Gain Of Function ◽

Tumor Bearing ◽

New Therapeutic Targets ◽

Low Expression ◽

Development Of Gastric Cancer

Aim: Our study aimed at investigating how LINC01133 functions in gastric cancer (GC) progression. Materials & methods: Gain-of-function and loss-of-function approaches were applied to analyze the effects of LINC01133, microRNA-576-5p (miR-576-5p) and somatostatin (SST) on the biological behaviors of GC cells and in tumor-bearing nude mice. Results: GC tissues and cells showed low expression of LINC01133, and LINC01133 overexpression decreased malignant phenotypes of GC cells. Moreover, LINC01133 upregulated SST through binding to miR-576-5p. Overexpressing miR-576-5p or suppressing SST reversed the functions of LINC01133 in biological potentials of GC cells and tumor growth. Conclusion: LINC01133 overexpression may inhibit GC development by downregulation of miR-576-5p and upregulation of SST, which suggests new therapeutic targets for GC.

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