MiR-30a-3p Suppresses the Growth and Development of Lung Adenocarcinoma Cells Through Modulating GOLM1/JAK-STAT Signaling

Ding, Dongxiao; Zhang, Yunqiang; Zhang, Xuede; Shi, Ke; Shang, Wenjun; Ying, Junjie; Wang, Li; Chen, Zhongjie; Hong, Haihua

doi:10.1007/s12033-022-00497-x

Cited by 3 publications

(3 citation statements)

References 38 publications

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“…Moreover, as GOLM1 affects the production of cytokines and chemokines, their autocrine signaling will likely also be affected, which in turn will affect downstream transcriptional processes. Indeed, overexpression of GOLM1 leads to increased signaling of JAK and STAT3 in the lung adenocarcinoma cell line A549, 46 possibly due to alterations in autocrine cytokine signaling. All these mechanisms likely contribute to the effects of GOLM1 on gene expression, 29 including downregulation of IFNB , 33,36 IL12A , 33,38 and upregulation of CXCL10 33 and CCL2 43 …”

Section: Discussionmentioning

confidence: 99%

“…The higher expression of GOLM1 is associated with decreased survival in lung cancer, melanoma, colorectal cancer, uveal melanoma and HCC 29,40,43,44 . As recently reviewed elsewhere, 9 GOLM1 expression can be increased by multiple extracellular factors in the tumor microenvironment, including hypoxia, 22 various miRNAs, 45–47 and the cytokines IL‐1β, 48 IL‐6 and Oncostatin M 49 . However, the upregulation of GOLM1 is not a universal phenomenon in cancer, because lower levels of GOLM1 have been reported in colon cancer 23 …”

Section: Golm1 Affects Cytokines In Cancermentioning

confidence: 99%

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Unveiling the impact of GOLM1/GP73 on cytokine production in cancer and infectious disease

et al. 2023

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The Golgi membrane protein GOLM1/GP73/GOLPH2 has been found to impact cytokine production in both infectious disease and cancer. In viral infections, GOLM1 levels are increased, and this lowers the production of type I interferons and other inflammatory cytokines. However, elevated GOLM1 expression levels due to mutations are linked to a higher production of interleukin (IL)‐6 during Candida infections, potentially explaining an increased susceptibility to candidemia in individuals carrying these mutations. In cancer, the protease Furin produces a soluble form of GOLM1 that has oncogenic properties by promoting the production of the chemokine CCL2 and suppressing the production of inflammatory cytokines such as IL‐12 and interferon gamma. This review will focus on the role of GOLM1 in cytokine production, highlighting how it can both promote and inhibit cytokine production. It is crucial to understand this in order to effectively target GOLM1 for therapeutic purposes in diseases associated with abnormal cytokine production, including cancer and infectious disease.

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Section: Discussionmentioning

confidence: 99%

Section: Golm1 Affects Cytokines In Cancermentioning

confidence: 99%

Unveiling the impact of GOLM1/GP73 on cytokine production in cancer and infectious disease

et al. 2023

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“…GP73 is involved in many human diseases, such as cancer, HIV, nonalcoholic fatty liver disease, and SARS-CoV-2-induced dysglycemia. [13][14][15][16][17][18] However, the role of GP73 in LPS-induced cardiac dysfunction remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Golgi Protein 73 Promotes LPS-Induced Cardiac Dysfunction via Mediating Myocardial Apoptosis and Autophagy

Xing,

Gao,

Bai

et al. 2024

Journal of Cardiovascular Pharmacology

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Sepsis-induced cardiac dysfunction represents a major cause of high mortality in intensive care units with limited therapeutic options. Golgi protein 73 (GP73) has been implicated in various diseases. However, the role of GP73 in LPS-induced cardiac dysfunction is unclear. Here, we established sepsis-induced cardiac dysfunction model by LPS administration in wild type (WT) and GP73 knockout (GP73 -/- ) mice. We found GP73 was increased in LPS-treated mouse hearts and LPS-cultured neonatal rat cardiomyocytes (NRCMs). Knockout of GP73 alleviated myocardial injury and improved cardiac dysfunction. Moreover, depletion of GP73 in NRCMs relieved LPS-induced cardiomyocyte apoptosis and activated myocardial autophagy. Therefore, GP73 is a negative regulator in LPS-induced cardiac dysfunction by promoting cardiomyocyte apoptosis and inhibiting cardiomyocyte autophagy.

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miR‐30a‐3p inhibits the proliferation of laryngeal cancer cells by targeting DNMT3a through regulating DNA methylation of PTEN

Gao,

Ren,

et al. 2023

Oncologie

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Objectives The study aims to examine how miR-30a-3p impacts the growth of laryngeal cancer by exploring its underlying mechanism. Our hypothesis suggests that the regulation of DNMT3a through PTEN by miR-30a-3p plays a significant role in the proliferation of laryngeal cancer. Methods To predict the role of miR-30a-3p in laryngeal cancer and its binding site to DNA methyltransferase 3a (DNMT3a), we utilized data from TCGA, GEO, and starBase. We employed Western blot and qRT-PCR to measure the expression levels of miR-30a-3p, DNMT3a, and PTEN. The interaction between miR-30a-3p and DNMT3a was evaluated using a Luciferase reporter assay. Cell proliferation and invasive abilities were assessed through the CCK-8 kit, EdU staining, and transwell assays. Results Analysis of TCGA data revealed that the expression of miR-30a-3p could impact the survival of patients with head and neck cancer. In Hep-2 cells, we observed down-regulated miR-30a-3p and up-regulated DNMT3a, with a negative correlation between the two. Furthermore, we discovered that miR-30a-3p directly targeted DNMT3a and suppressed its expression in Hep-2 cells, resulting in a decrease in cellular proliferation and invasive capabilities. Additionally, overexpression of miR-30a-3p in Hep-2 cells activated PTEN by reducing DNMT3a expression. Conclusions Our findings indicate that miR-30a-3p, acting as a tumor suppressor gene, plays a regulatory role in the growth and progression of laryngeal cancer through its interaction with DNMT3a and PTEN.

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MiR-30a-3p Suppresses the Growth and Development of Lung Adenocarcinoma Cells Through Modulating GOLM1/JAK-STAT Signaling

Cited by 3 publications

References 38 publications

Unveiling the impact of GOLM1/GP73 on cytokine production in cancer and infectious disease

Unveiling the impact of GOLM1/GP73 on cytokine production in cancer and infectious disease

Golgi Protein 73 Promotes LPS-Induced Cardiac Dysfunction via Mediating Myocardial Apoptosis and Autophagy

miR‐30a‐3p inhibits the proliferation of laryngeal cancer cells by targeting DNMT3a through regulating DNA methylation of PTEN

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