scholarly journals Silencing ELMO3 Inhibits the Growth, Invasion, and Metastasis of Gastric Cancer

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Yan Hu ◽  
Qiongfang Yu ◽  
Yao Zhong ◽  
Wei Shen ◽  
Xiaoyan Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Actin Polymerization ◽  
Vital Role ◽  
Gastric Cancer Cells ◽  
Invasion And Migration ◽  
Real Time Quantitative Pcr ◽  
And Migration

ELMO3 is a member of the engulfment and cell motility (ELMO) protein family, which plays a vital role in the process of chemotaxis and metastasis of tumor cells. However, remarkably little is known about the role of ELMO3 in cancer. The present study was conducted to investigate the function and role of ELMO3 in gastric cancer (GC) progression. The expression level of ELMO3 in gastric cancer tissues and cell lines was measured by means of real-time quantitative PCR (qPCR) and Western blot analysis. RNA interference was used to inhibit ELMO3 expression in gastric cancer cells. Then, wound-healing assays, Transwell assays, MTS assays, flow cytometry, and fluorescence microscopy were applied to detect cancer cell migration, cell invasion, cell proliferation, the cell cycle, and F-actin polymerization, respectively. The results revealed that ELMO3 expression in GC tumor tissues was significantly higher than in the paired adjacent tissues. Moreover, knockdown of ELMO3 by a specific siRNA significantly inhibited the processes of cell proliferation, invasion, metastasis, regulation of the cell cycle, and F-actin polymerization. Collectively, the results indicate that ELMO3 participates in the processes of cell growth, invasion, and migration, and ELMO3 is expected to be a potential diagnostic and prognostic marker for GC.

156 THE EXPRESSION AND ROLE OF ANO9 IN HUMAN ESOPHAGEAL SQUAMOUS CELL CARCINOMA

2021 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Hiroyuki Inoue ◽  
Atsushi Shiozaki ◽  
Hitoshi Fujiwara ◽  
Hirotaka Konishi ◽  
Keita Katsurahara ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Prognostic Factor ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Microarray Analysis ◽  
Invasion And Migration ◽  
And Migration

Abstract   The anoctamin (ANO) family consists of transmembrane proteins in 10 isoforms, and ANOs are broadly expressed in epithelial and non-epithelial tissues. Few studies have reported the function and activation mechanism of ANO9 in esophageal squamous cell carcinoma (ESCC), and the clinical significance of its expression remains unclear. The aims of the present study were to investigate the role of ANO9 in the regulation of tumor progression and its clinicopathological significance in ESCC. Methods In human ESCC cell lines KYSE150 and KYSE790, knockdown experiments were performed using ANO9 siRNA, and the effects on cell proliferation, cell cycle, apoptosis, invasion and migration were analyzed. The gene expression profiles of cells were examined using a microarray analysis. Immunohistochemical (IHC) analysis was performed on 57 primary tumor samples obtained from ESCC patients who underwent curative esophagectomy between 1999 and 2009 in Kyoto Prefectural University of Medicine. Results In an in vitro study, the depletion of ANO9 reduced cell proliferation, invasion and migration in KYSE150 and KYSE 790 cells. And, the depletion of ANO9 increased the number of cells in G0/G1 arrest and induced apoptosis in these cells. The results of the microarray analysis indicated that various centrosome-related genes such as CEP120, CNTRL and SPAST, were up- or down-regulated in ANO9-depleted KYSE150 cells. The IHC results showed that high expression of ANO9 was independent prognostic factor in ESCC patients (p = 0.025). Conclusion ANO9 played the important role in the cell cycle and progression of ESCC cells through the expression of centrosome-related genes. In addition, the high expression of ANO9 was a poor prognostic factor in ESCC patients. The results of the present study indicate that ANO9 has potential as a biomarker for cancer growth and as a therapeutic target for ESCC such as inhibitor or RNA interference of ANO9.

scholarly journals Role of miR-96 in invasion and migration of gastric cancer cells

2013 ◽  
Vol 21 (34) ◽  
pp. 3775
Author(s):  
Sheng-Xun Mao ◽  
Zhi-Yong Zhou ◽  
Nan He ◽  
Cheng-Long Yin ◽  
Jia-Qing Cao
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals YWHAE silencing induces cell proliferation, invasion and migration through the up-regulation of CDC25B and MYC in gastric cancer cells: new insights about YWHAE role in the tumor development and metastasis process

Oncotarget ◽  
2016 ◽  
Vol 7 (51) ◽  
pp. 85393-85410 ◽  
Author(s):  
Mariana Ferreira Leal ◽  
Helem Ferreira Ribeiro ◽  
Juan Antonio Rey ◽  
Giovanny Rebouças Pinto ◽  
Marília Cardoso Smith ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Tumor Development ◽  
Gastric Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

Effects and Mechanisms of Anlotinib and Dihydroartemisinin Combination Therapy in Ameliorating Malignant Biological Behavior of Gastric Cancer Cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Qiong Luo ◽  
Suyun Zhang ◽  
Donghuan Zhang ◽  
Rui Feng ◽  
Nan Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Chorioallantoic Membrane ◽  
Cell Counting ◽  
Biological Behavior ◽  
Gastric Cancer Cells ◽  
Invasion And Migration ◽  
Apoptosis Related Protein ◽  
And Migration

Background: Gastric cancer(GC) is currently one of the major malignancies that threatens human lives and health. Anlotinib is a novel small-molecule that inhibits angiogenesis to exert anti-tumor effects. However, the function in gastric cancer is incompletely understood. Objective: The aim of the present study was to investigate the anti-tumor effects and molecular mechanisms of anlotinib combined with dihydroartemisinin (DHA) in SGC7901 gastric cancer cells. Method: Different concentrations of anlotinib and DHA were used to treat SGC7901 gastric cancer cells, after which cell proliferation was measured. Drug interactions of anlotinib and DHA were analyzed by the Chou-Talalay method with CompuSyn software. proliferation, apoptosis, invasion, migration, and angiogenesis were measured using the cell counting kit-8 (CCK8) assay, flow cytometry, Transwell invasion assays, scratch assays, and chicken chorioallantoic membrane (CAM) assays. proliferation-associated protein (Ki67), apoptosis-related protein (Bcl-2), and vascular endothelial growth factor A (VEGF-A) were quantified by Western bloting. Results: The combination of 2.5 μmol/L of anlotinib and 5 of μmol/L DHA was highly synergistic in inhibiting cell growth, significantly increased the apoptosis rate and suppressed obviously the invasion and migration capability and angiogenesis of gastric cancer cells. In addition, the expression levels of Ki67, Bcl-2, and VEGF-A, as well as angiogenesis, were significantly decreased in the Combination of drugs compared with in control and either drug alone. Conclusion: The combination of anlotinib and DHA showed synergistic antitumor activity, suggesting their potential in treating patients with gastric cancer.

scholarly journals The tRNA-derived fragment 5026a inhibits the proliferation of gastric cancer cells by regulating the PTEN/PI3K/AKT signaling pathway

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Linwen Zhu ◽  
Zhe Li ◽  
Xiuchong Yu ◽  
Yao Ruan ◽  
Yijing Shen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Gastric Cancer Cells ◽  
Qrt Pcr

Abstract Background Recently, tRNA-derived fragments (tRFs) have been shown to serve important biological functions. However, the role of tRFs in gastric cancer has not been fully elucidated. This study aimed to identify the tumor suppressor role of tRF-5026a (tRF-18-79MP9P04) in gastric cancer. Methods Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was first used to detect tRF-5026a expression levels in gastric cancer tissues and patient plasma. Next, the relationship between tRF-5026a levels and clinicopathological features in gastric cancer patients was assessed. Cell lines with varying tRF-5026a levels were assessed by measuring tRF-5026a using qRT-PCR. After transfecting cell lines with a tRF-5026a mimic or inhibitor, cell proliferation, colony formation, migration, apoptosis, and cell cycle were evaluated. The expression levels of related proteins in the PTEN/PI3K/AKT pathway were also analyzed by Western blotting. Finally, the effect of tRF-5026a on tumor growth was tested using subcutaneous tumor models in nude mice. Results tRF-5026a was downregulated in gastric cancer patient tissues and plasma samples. tRF-5026a levels were closely related to tumor size, had a certain diagnostic value, and could be used to predict overall survival. tRF-5026a was also downregulated in gastric cancer cell lines. tRF-5026a inhibited the proliferation, migration, and cell cycle progression of gastric cancer cells by regulating the PTEN/PI3K/AKT signaling pathway. Animal experiments showed that upregulation of tRF-5026a effectively inhibited tumor growth. Conclusions tRF-5026a (tRF-18-79MP9P04) is a promising biomarker for gastric cancer diagnostics and has tumor suppressor effects mediated through the PTEN/PI3K/AKT signaling pathway.

scholarly journals FGFR3 promotes the growth and malignancy of melanoma by influencing EMT and the phosphorylation of ERK, AKT, and EGFR

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Lei Li ◽  
Shuai Zhang ◽  
Hao Li ◽  
Haiyan Chou
Keyword(s):  
Cell Proliferation ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Colony Formation ◽  
Caspase 3 ◽  
Growth Factor Receptor ◽  
Invasion And Migration ◽  
Node Metastasis ◽  
And Migration

Abstract Background Overexpression of fibroblast growth factor receptor 3 (FGFR3) has been linked to tumor progression in many types of cancer. The role of FGFR3 in melanoma remains unclear. In this study, we aimed to uncover the role of FGFR3 in the growth and metastasis of melanoma. Methods FGFR3 knockdown and overexpression strategies were employed to investigate the effects of FGFR3 on colony formation, cell apoptosis, proliferation, migration, and in vitro invasion, along with the growth and metastasis of melanoma in a xenografts mouse model. The protein expression levels of extracellular signal-regulated kinase (ERK), protein kinase B (AKT), epidermal growth factor receptor (EGFR), and epithelial-mesenchymal transition (EMT) markers were determined by Western blot analysis. Results The mRNA expression of FGFR3 was higher in melanoma tissues than normal healthy tissues. FGFR3 expression in cutaneous malignant melanoma (CMM) tissues was positively correlated with the Breslow thickness and lymph node metastasis. In A357 cells, knockdown of the FGFR3 gene decreased the colony formation ability, cell proliferation, invasion, and migration, but increased the caspase 3 activity and the apoptosis rate; overexpression of FGFR3 increased the colony formation ability, cell proliferation, invasion, and migration, but decreased the caspase 3 activity and apoptosis rates. FGFR3 knockdown also upregulated E-cadherin, downregulated N-cadherin and vimentin, and decreased the phosphorylation levels of ERK, AKT, and EGFR. In the MCC xenografts mice, knockdown of FGFR3 decreased tumor growth and metastasis. Conclusions FGFR3, which is highly expressed in CMM tissues, is correlated with increased Breslow thickness and lymph node metastasis. FGFR3 promotes melanoma growth, metastasis, and EMT behaviors, likely by affecting the phosphorylation levels of ERK, AKT, and EGFR.

The Role of Cancer-associated Fibroblasts in Tumorigenesis of Gastric Cancer

2018 ◽  
Vol 24 (28) ◽  
pp. 3297-3302 ◽  
Author(s):  
Zhilong Ma ◽  
Min Chen ◽  
Xiaohu Yang ◽  
Bin Xu ◽  
Zhenshun Song ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Tumor Biology ◽  
Vital Role ◽  
Cancer Associated Fibroblasts ◽  
Gastric Cancer Cells ◽  
Stromal Fibroblasts ◽  
Tumor Microenvironments ◽  
Tumorigenesis And Progression

Cancer-associated fibroblasts (CAFs) are an important cell type present in solid tumor microenvironments, including that of gastric cancer. They play a vital role in the promotion of tumorigenesis, angiogenesis, and cancer progression through paracrine signaling and modulation of the extracellular matrix. However, the exact molecular mechanism underlying the interaction between gastric cancer cells and stromal fibroblasts remains poorly understood. Recent studies have demonstrated that various factors, such as gene and microRNA variations, are involved in this process. This review discusses recent advances in understanding how these factors are regulated in CAFs and how they affect tumor biology, which may improve our understanding of their role in gastric cancer tumorigenesis and progression and provide new promising targets for therapeutic strategies.

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