Overexpression of SSH1 in gastric adenocarcinoma and its correlation with clinicopathological features

Daryabari, Seyedeh Saideh; Safaralizadeh, Reza; Feizi, Mohammad Ali Hosseinpour; Moaddab, Yaghoub; Shokouhi, Behrooz

doi:10.21037/jgo.2018.03.09

Cited by 11 publications

(6 citation statements)

References 22 publications

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“…Given that persistent stimulation by H. pylori lysate exposure promoted proliferation and inhibited autophagy and apoptosis of GES-1 cells, we hypothesized that the treatment could promote the tendency for malignant progression. We detected the mRNA expression level of three gastric cancer biomarkers, chloride channel-3 (CLC-3), slingshot protein phosphatase 1 (SSH1), and sirtuin 4 (SIRT4) (33)(34)(35) in Cul 30 -GES-1 and B-GES-1 cells. We found that the mRNA levels of SSH1 and CLC3 increased significantly, while SIRT4 decreased, compared with the control group (Figures 4G-I).…”

Section: Constant Treatment Of H Pylori Lysate Inhibited Apoptosis Of Ges-1 Cells and Contributed To A Tendency For Cell Cancerationmentioning

confidence: 99%

Sustained Exposure to Helicobacter pylori Lysate Inhibits Apoptosis and Autophagy of Gastric Epithelial Cells

Wang

Zhang

et al. 2020

Front. Oncol.

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Helicobacter pylori is designated as a class I carcinogen of human gastric cancer following long-term infection. During this process, H. pylori bacteria persist in proliferation and death, and release bacterial components that come into contact with gastric epithelial cells and regulate host cell function. However, the impact of long-term exposure to H. pylori lysate on the pathological changes of gastric cells is not clear. In this study, we aimed to investigate the regulation and mechanisms involved in gastric cell dysfunction following continuous exposure to H. pylori lysate. We co-cultured gastric cell lines GES-1 and MKN-45 with H. pylori lysate for 30 generations, and we found that sustained exposure to H. pylori lysate inhibited GES-1 cell invasion, migration, autophagy, and apoptosis, while it did not inhibit MKN-45 cell invasion or migration. Furthermore, Mongolian gerbils infected with H. pylori ATCC 43504 strains for 90 weeks confirmed the in vitro results. The clinical and in vitro data indicated that sustained exposure to H. pylori lysate inhibited cell apoptosis and autophagy through the Nod1-NF-kB/MAPK-ERK/FOXO4 signaling pathway. In conclusion, sustained exposure to H. pylori lysate promoted proliferation of gastric epithelial cells and inhibited autophagy and apoptosis via Nod1-NF-kB/MAPK-ERK/FOXO4 signaling pathway. In the process of H. pylori-induced gastric lesions, H. pylori lysate plays as an "accomplice" to carcinogenesis.

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Section: Constant Treatment Of H Pylori Lysate Inhibited Apoptosis Of Ges-1 Cells and Contributed To A Tendency For Cell Cancerationmentioning

confidence: 99%

Sustained Exposure to Helicobacter pylori Lysate Inhibits Apoptosis and Autophagy of Gastric Epithelial Cells

Wang

Zhang

et al. 2020

Front. Oncol.

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“…Gastric cancer, currently, is the fourth most prevalent cancer and the second most fatal cause of death in the world (Mohammadi et al, 2015). Unfortunately, its symptoms are usually diagnosed when the disease has advanced and is in a metastatic state (Daryabari, Safaralizadeh, Hosseinpourfeizi, Moaddab, & Shokouhi, 2018). Therefore, preventing this disease is an important treatment strategy (Okimoto et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

“…Different types of therapeutic strategies, such as surgery, chemotherapy, and radiation, are considered for the treatment of gastric cancer, but they are not effective due to lack of early‐stage diagnosis, tumor invasion, and metastasis (Daryabari et al, 2018). Then, it is necessary to improve the therapeutic index and identify new treatment strategies (Yang et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…The actin protein network has been recognized as the base engine for cellular mobility and metastasis (Vindin & Gunning, 2013). CFL1, as a protein that regulates actin polymerization and depolymerization (Wang, Eddy, & Condeelis, 2007), has a significant role in the progression and metastasis of cancer cells (Daryabari et al, 2018;Wang et al, 2006). CFL1, a family member of ADF, encodes a small ubiquitous protein (Lu, Fu, Luo, Li, & Li, 2015) with the weight of 19 kDa, (Bamburg, McGough, & Ono, 1999) which binds to G-actin and F-actin and then inhibits polymerization of G-actin in a pH-dependent manner (Ono, 2007).…”

mentioning

confidence: 99%

“…Unfortunately, its symptoms are usually diagnosed when the disease has advanced and is in a metastatic state (Daryabari, Safaralizadeh, Hosseinpourfeizi, Moaddab, & Shokouhi, 2018). Therefore, preventing this disease is an important treatment strategy (Okimoto et al, 2017).…”

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confidence: 99%

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Overexpression of CFL1 in gastric cancer and the effects of its silencing by siRNA with a nanoparticle delivery system in the gastric cancer cell line

Daryabari

Fathi

Mahdavi

et al. 2020

Journal Cellular Physiology

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Gastric adenocarcinoma, like other cancers, is a multifactorial genetic disease, and metastasis of cancer cells is one of the main features of this illness. The expression levels of the CFL1 gene have been modulated in this pathway. Using small interfering RNA (siRNA) in the treatment of gastric cancer is considered a hopeful gene therapeutic approach. The present study reported the level of CFL1 genes between tumor and margin and healthy tissue of gastric cancer. Also, the features of a cationic nanoparticle with a polymer coating containing polyacrylic acid and polyethyleneimine that were used in the delivery of CFL1 siRNA, were shown. Then the cytotoxicity, cellular uptake, and gene silencing efficiency of this nanoparticle were evaluated with CFL1siRNA.Method: In this study, the CFL1 gene expression was measured in 40 gastric adenocarcinoma, marginal and 15 healthy biopsy samples by a real-time polymerase chain reaction. Physicochemical characteristics, apoptosis, and inhibition of migration of the delivery of CFL1 siRNA by nanoparticle and lipofectamine were investigated in gastric cancer cells.Result: The CFL1 expression was remarkably increased in gastric cancer tissues in comparison with the marginal samples and normal tissues (p < .05) and the biomarker index for CFL1 was obtained as 0.94, then this gene can be probably used as a biomarker for gastric cancer. After treatment of the AGS cell line by CFL1 siRNA, the CFL1 expression level of mRNA and migration in AGS cells were remarkably suppressed after transfection. Furthermore, the amount of apoptosis increased (p < .05). Conclusion:Our results demonstrated that CFL1 downregulation in AGS cells can interdict cell migration. Finally, our outcomes propose that CFL1 can function as an oncogenic gene in gastric cancer and would be considered as a potential purpose of gene therapy for gastric cancer treatment.

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Expression profiles of miR-196, miR-132, miR-146a, and miR-134 in human colorectal cancer tissues in accordance with their clinical significance

Maralani

Shanehbandi

Asadi

et al. 2021

Wien Klin Wochenschr

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Overexpression of SSH1 in gastric adenocarcinoma and its correlation with clinicopathological features

Abstract: The results obtained from investigating SSH1 expression are indicative of significant changes in the expression of this gene in gastric adenocarcinoma. This gene can also be used as a biomarker for gastric cancer.

Cited by 11 publications

References 22 publications

Sustained Exposure to Helicobacter pylori Lysate Inhibits Apoptosis and Autophagy of Gastric Epithelial Cells

Sustained Exposure to Helicobacter pylori Lysate Inhibits Apoptosis and Autophagy of Gastric Epithelial Cells

Overexpression of CFL1 in gastric cancer and the effects of its silencing by siRNA with a nanoparticle delivery system in the gastric cancer cell line

Expression profiles of miR-196, miR-132, miR-146a, and miR-134 in human colorectal cancer tissues in accordance with their clinical significance

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