SOCS3 gene silencing does not occur through methylation and mutations in gastric cancer

Saqri, Atika Al; Malgundkar, Shika Hanif; Kindi, Fatima Al; Gupta, Ishita; Al-Moundhri, Mansour; Tamimi, Yahya

doi:10.1007/s13577-022-00715-3

Cited by 4 publications

(3 citation statements)

References 50 publications

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“…Administration of antileptin antibodies diminished gastric mucosa hyperplasia, indicating that targeting the leptin/ObRb/STAT3 axis can be a potential therapeutic strategy for GC [88]. In addition, it was indicated that the expression of SOCS3 was downregulated after silencing lncRNA AC125807.2 in a human GC cell line, indicating the possible involvement of lncRNA AC125807.2 in regulation of SOCS3 expression [89]. Moreover, DNA methylation of the SOCS3 gene is a key epigenetic alteration supporting GC development [30,90].…”

Section: Socs3 Role In Gc and Factors Influencing Socs3 Expression In Gcmentioning

confidence: 99%

The Interplay Between Helicobacter pylori and Suppressors of Cytokine Signaling (SOCS) Molecules in the Development of Gastric Cancer and Induction of Immune Response

Jafarzadeh,

Nemati

et al. 2024

Helicobacter

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Helicobacter pylori (H. pylori) colonizes the stomach and leads to the secretion of a vast range of cytokines by infiltrated leukocytes directing immune/inflammatory response against the bacterium. To regulate immune/inflammatory responses, suppressors of cytokine signaling (SOCS) proteins bind to multiple signaling components located downstream of cytokine receptors, such as Janus kinase (JAK), signal transducers and activators of transcription (STAT). Dysfunctional SOCS proteins in immune cells may facilitate the immune evasion of H. pylori, allowing the bacteria to induce chronic inflammation. Dysregulation of SOCS expression and function can contribute to the sustained H. pylori‐mediated gastric inflammation which can lead to gastric cancer (GC) development. Among SOCS molecules, dysregulated expression of SOCS1, SOCS2, SOCS3, and SOCS6 were indicated in H. pylori‐infected individuals as well as in GC tissues and cells. H. pylori‐induced SOCS1, SOCS2, SOCS3, and SOCS6 dysregulation can contribute to the GC development. The expression of SOCS molecules can be influenced by various factors, such as epigenetic DNA methylation, noncoding RNAs, and gene polymorphisms. Modulation of the expression of SOCS molecules in gastric epithelial cells and immune cells can be considered to control gastric carcinogenesis as well as regulate antitumor immune responses, respectively. This review aimed to explain the interplay between H. pylori and SOCS molecules in GC development and immune response induction as well as to provide insights regarding potential therapeutic strategies modulating SOCS molecules.

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Section: Socs3 Role In Gc and Factors Influencing Socs3 Expression In Gcmentioning

confidence: 99%

The Interplay Between Helicobacter pylori and Suppressors of Cytokine Signaling (SOCS) Molecules in the Development of Gastric Cancer and Induction of Immune Response

Jafarzadeh,

Nemati

et al. 2024

Helicobacter

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“…Few mutations in the SOCS3 gene have been described in humans. Several cases of gastric cancer have been reported, that seem to be more related to non-coding RNA-mediated gene silencing processes than to methylations affecting the functionality of SOCS3 [ 36 ]. In oncogenic diseases, such as glioblastoma multiforme, an increase in methylation of the SOCS3 gene has been detected, with a subsequent decrease in its expression [ 37 ], whereas overexpression of SOCS3 has been associated with changes in circulating miRNAs in children with obesity [ 38 ].…”

Section: Regulation Of Leptin Efficiencymentioning

confidence: 99%

“…In addition, these authors found that some targets of let-7 presented SNPs that were related to changes in the control of fasting glucose and T2DM [ 202 ]. Moreover, miR-26b is downregulated by leptin [ 36 ] and this miRNA was found to be reduced in visceral adipose tissue (VAT) in insulin-resistant adipocytes, obese rodent models, and human obesity [ 203 ]. Insulin-stimulated glucose uptake is promoted by miR-26b, as well as the translocation of insulin-stimulated glucose transporter type 4 to the plasma membrane in mature human adipocytes.…”

Section: Functionality Of Leptin and Its Involvement In Pathologymentioning

confidence: 99%

Recent Advances in the Knowledge of the Mechanisms of Leptin Physiology and Actions in Neurological and Metabolic Pathologies

Casado

Collado-Pérez

Frago

et al. 2023

IJMS

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Excess body weight is frequently associated with low-grade inflammation. Evidence indicates a relationship between obesity and cancer, as well as with other diseases, such as diabetes and non-alcoholic fatty liver disease, in which inflammation and the actions of various adipokines play a role in the pathological mechanisms involved in these disorders. Leptin is mainly produced by adipose tissue in proportion to fat stores, but it is also synthesized in other organs, where leptin receptors are expressed. This hormone performs numerous actions in the brain, mainly related to the control of energy homeostasis. It is also involved in neurogenesis and neuroprotection, and central leptin resistance is related to some neurological disorders, e.g., Parkinson’s and Alzheimer’s diseases. In peripheral tissues, leptin is implicated in the regulation of metabolism, as well as of bone density and muscle mass. All these actions can be affected by changes in leptin levels and the mechanisms associated with resistance to this hormone. This review will present recent advances in the molecular mechanisms of leptin action and their underlying roles in pathological situations, which may be of interest for revealing new approaches for the treatment of diseases where the actions of this adipokine might be compromised.

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The pivotal role of long non-coding RNAs as potential biomarkers and modulators of chemoresistance in ovarian cancer (OC)

Malgundkar,

Tamimi

2024

Hum. Genet.

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SOCS3 gene silencing does not occur through methylation and mutations in gastric cancer

Cited by 4 publications

References 50 publications

The Interplay Between Helicobacter pylori and Suppressors of Cytokine Signaling (SOCS) Molecules in the Development of Gastric Cancer and Induction of Immune Response

The Interplay Between Helicobacter pylori and Suppressors of Cytokine Signaling (SOCS) Molecules in the Development of Gastric Cancer and Induction of Immune Response

Recent Advances in the Knowledge of the Mechanisms of Leptin Physiology and Actions in Neurological and Metabolic Pathologies

The pivotal role of long non-coding RNAs as potential biomarkers and modulators of chemoresistance in ovarian cancer (OC)

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