scholarly journals Golgi phosphoprotein-3 promotes invasiveness of gastric cancer cells through the mTOR signalling pathway

2019 ◽  
Vol 42 (2) ◽  
pp. E38-47 ◽  
Author(s):  
Jun Liu ◽  
Hongquan Wei ◽  
Liqin Lai ◽  
Yuanyuan Wang ◽  
Xiaoyu Han ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cell Invasion ◽  
Signalling Pathway ◽  
Gastric Cancer Cells ◽  
Poorly Differentiated ◽  
The Impact ◽  
Mtor Signalling ◽  
Mtor Signalling Pathway

Purpose: Golgi phosphoprotein-3 (GOLPH3) is an oncogene that is overexpressed in multiple cancers and is associated with poor prognosis. The aim of this study was to examine the impact of GOLPH3 on the migration and metastasis of gastric cancer cells. Methods: Following the shRNA-mediated knockdown of GOLPH3, we analyzed cytoskeletal reorganization and cell invasion, migration and adhesion, and determined the impact of components of the mammalian target of the rapamycin (mTOR) signalling pathway. Results: The GOLPH3 mRNA and protein expression were significantly lower in both SGC-7901 and MKN-28 cells as compared with poorly-differentiated BGC-823 cells. The GOLPH3 knockdown also significantly reduced cell invasion in all three cell lines through reduced migration as compared with the non-targeting control sequence group. The GOLPH3 knockdown also reduced F-actin in all three cell lines, and decreased cell adhesion in BGC-823 and SGC-7901 cells. Finally, p-mTOR, p70S6K, p-4EBP1 and RhoA protein levels were significantly downregulated in shGOLPH3-1-treated cells. Conclusions: In conclusion, GOLPH3 increased in poorly-differentiated gastric cancer cells, activating the mTOR-70S6K/4EBP1-RhoA signalling pathway to promote the migration and metastasis of gastric cancer cells.

scholarly journals Inhibition of mTOR-Akt-ULK1 signaling pathway and activation of autophagy by TNFAIP8 in metastasis of gastric cancer

2020 ◽  
Author(s):  
Zheng Chen ◽  
Jianguo Zhang ◽  
Chenyang Dong ◽  
Dongsheng Li ◽  
Yuehan Yin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cell Invasion ◽  
Gastric Cancer Cell ◽  
Signal Pathway ◽  
Rt Pcr ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
A Cell

Abstract Background The purpose of this article is to study the mechanism of TNFAIP8 in gastric cancer. Methods RT-PCR was used to detect the expression of TNFAIP8 mRNA in normal gastric mucosa cells and four gastric cancer cell lines. TNFAIP8 was silenced or overexpressed in two cell lines, CCK-8 cell viability was used, transwell experiment was used to detect cell invasion capability, and flow cytometry was used to detect cell apoptosis. TNFAIP was silenced or overexpressed in a cell line, and nude mice were inoculated to form transplanted tumors. HE staining and immunohistochemistry staining were used to detect the histopathological changes of tumors. Results The expression of TNFAIP8 was significantly up-regulated in GC patients and cells. After silencing and overexpressing TNFAIP8, gastric cancer cells with high expression increased, apoptosis decreased, and cell invasion increased. Expression of mTOR-Akt-ULK1 signal pathway was inhibited and autophagy signal was activated. Conclusions Our findings indicate that TNFAIP8 inhibits the metastasis of gastric cancer cells by inhibiting mTOR-Akt-ULK1 signal pathway and activating autophagy signal.

scholarly journals The role of TNFAIP8-mediated mTOR-Akt-ULK1 signaling pathway in gastric cancer

2020 ◽  
Author(s):  
Zheng Chen ◽  
Jianguo Zhang ◽  
Chenyang Dong ◽  
Dongsheng Li ◽  
Yuehan Yin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cell Invasion ◽  
Signal Pathway ◽  
Gastric Cancer Cells ◽  
Mrna And Protein Expression ◽  
Gastric Cancer Cell Lines ◽  
A Cell

Abstract Background: The purpose of this article was to study the role of TNFAIP8 in gastric cancer. Methods: RT-PCR was used to detect the expression of TNFAIP8 mRNA and protein level in normal gastric mucosa cells and four gastric cancer cell lines. TNFAIP8 was silenced or overexpressed in two cell lines, CCK-8 cell viability was used, transwell experiment was used to detect cell invasion capability, and flow cytometry was used to detect cell apoptosis. TNFAIP was silenced or overexpressed in a cell line, and nude mice were inoculated to form transplanted tumors. HE staining and immunohistochemistry staining were used to detect the histopathological changes of tumors. Results: The mRNA and protein expression of TNFAIP8 was significantly up-regulated in GC patients and cells. After silencing and overexpressing TNFAIP8, gastric cancer cells with high expression increased, apoptosis decreased, and cell invasion increased. Expression of mTOR-Akt-ULK1 signal pathway was inhibited and autophagy signal was activated. Conclusions: Our findings indicate that TNFAIP8 inhibited gastric cancer cells by inhibiting mTOR-Akt-ULK1 signal pathway and activating autophagy signal.

scholarly journals TNFAIP8 inhibits the proliferation of gastric cancer cells by inhibiting mTOR-Akt-ULK1 signal pathway and activating autophagy

2020 ◽  
Author(s):  
Zheng Chen ◽  
Jianguo Zhang ◽  
Chenyang Dong ◽  
Dongsheng Li ◽  
Yuehan Yin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cell Invasion ◽  
Signal Pathway ◽  
Gastric Cancer Cells ◽  
Mrna And Protein Expression ◽  
Gastric Cancer Cell Lines ◽  
A Cell

Abstract Background : The purpose of this article was to study the role of TNFAIP8 in gastric cancer. Methods : RT-PCR was used to detect the expression of TNFAIP8 mRNA and protein level in normal gastric mucosa cells and four gastric cancer cell lines. TNFAIP8 was silenced or overexpressed in two cell lines, CCK-8 cell viability was used, transwell experiment was used to detect cell invasion capability, and flow cytometry was used to detect cell apoptosis. TNFAIP was silenced or overexpressed in a cell line, and nude mice were inoculated to form transplanted tumors. HE staining and immunohistochemistry staining were used to detect the histopathological changes of tumors. Results : The mRNA and protein expression of TNFAIP8 was significantly up-regulated in GC patients and cells. After silencing and overexpressing TNFAIP8, gastric cancer cells with high expression increased, apoptosis decreased, and cell invasion increased. Expression of mTOR-Akt-ULK1 signal pathway was inhibited and autophagy signal was activated. Conclusions : Our findings indicate that TNFAIP8 inhibited gastric cancer cells by inhibiting mTOR-Akt-ULK1 signal pathway and activating autophagy signal.

scholarly journals Calponin 3 Regulates Cell Invasion and Doxorubicin Resistance in Gastric Cancer

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Keun-Seok Hong ◽  
Hyemin Kim ◽  
Seon-Hee Kim ◽  
Minju Kim ◽  
Jiyun Yoo
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Cancer Cell Lines ◽  
Chemotherapeutic Agents ◽  
Actin Binding ◽  
Gastric Cancer Cells ◽  
Doxorubicin Resistance

Calponin 3 (CNN3) is an F-actin-binding protein that regulates actin cytoskeletal rearrangement. However, the role of CNN3 in cancer cell invasion and resistance to chemotherapeutic agents has not yet been investigated. The present study was undertaken to investigate whether CNN3 influences cancer-related phenotypes in gastric cancer. We demonstrate that CNN3 contributes to cell invasion and resistance to doxorubicin in gastric cancer. CNN3 expression was markedly elevated in highly invasive cancer cell lines compared to less invasive or noninvasive cancer cell lines. Depletion of CNN3 protein suppressed the invasive ability of gastric cancer cells. The highly invasive MKN-28 gastric cancer cells were more resistant to doxorubicin than the noninvasive MKN-45 cells; however, knockdown of CNN3 expression in MKN-28 cells resensitized them to doxorubicin treatment. Taken together, our results suggest that CNN3 plays a key role in invasiveness and doxorubicin resistance in gastric cancer cells.

scholarly journals Distinctive Prognostic Value and Cellular Functions of Osteopontin Splice Variants in Human Gastric Cancer

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1820
Author(s):  
Chengcheng Hao ◽  
Yuxin Cui ◽  
Jane Lane ◽  
Shuqin Jia ◽  
Jiafu Ji ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Prognostic Value ◽  
Splice Variants ◽  
Tnm Staging ◽  
Migration And Invasion ◽  
Ros Production ◽  
Gastric Cancer Cells ◽  
Normal Tissues

Background: Osteopontin (OPN) splice variants are identified as predictors of tumour progression and therapeutic resistance in certain types of solid tumours. However, their roles in gastric cancer (GC) remain poorly characterized. The current study sought to assess the prognostic value of the three OPN splice variants (namely OPN-a, OPN-b, and OPN-c) in gastric cancer and their potential functions within gastric cancer cells. Methods: RNA extraction and reverse transcription were performed using our clinical cohort of gastric carcinomas and matched normal tissues (n = 324 matched pairs). Transcript levels were determined using real-time quantitative PCR. Three OPN splice variants overexpressed cell lines were created from the gastric cancer cell line HGC-27. Subsequently, biological functions, including cell growth, adhesion, migration, and invasion, were studied. The potential effects of OPN isoforms on cisplatin and 5-Fu were evaluated by detecting cellular reactive oxygen species (ROS) levels in the HGC-27-derived cell lines. Results: Compared with normal tissues, the expression levels of three splice variants were all elevated in gastric cancer tissues in an order of OPN-a > OPN-b > OPN-c. The OPN-a level significantly increased with increasing TNM staging and worse clinical outcome. There appeared to be a downregulation for OPN-c in increasing lymph node status (p < 0.05), increasing TNM staging, and poor differentiation. High levels of OPN-a and OPN-b were correlated with short overall survival and disease-free survival of gastric cancer patients. However, the low expression of OPN-c was significantly associated with a poor prognosis. Functional analyses further showed that ectopic expression of OPN-c suppressed in vitro proliferation, adhesiveness, migration, and invasion properties of HGC-27 cells, while the opposite role was seen for OPN-a. Cellular ROS detection indicated that OPN-a and OPN-c significantly promoted ROS production after treatment with 5-Fu comparing to OPN-vector, while only OPN-a markedly induced ROS production after treatment with cisplatin. Conclusion: Our results suggest that OPN splice variants have distinguished potential to predict the prognosis of gastric cancer. Three OPN variants exert distinctive functions in gastric cancer cells. Focusing on specific OPN isoforms could be a novel direction for developing diagnostic and therapeutic approaches in gastric cancer.

scholarly journals Sevoflurane represses the migration and invasion of gastric cancer cells by regulating forkhead box protein 3

2021 ◽  
Vol 49 (4) ◽  
pp. 030006052110059
Author(s):  
Fangfang Yong ◽  
Hemei Wang ◽  
Chao Li ◽  
Huiqun Jia
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Control Group ◽  
Gastric Cancer Cells ◽  
Cell Migration And Invasion ◽  
Forkhead Box ◽  
Induced Apoptosis

Objective Previous studies suggested that sevoflurane exerts anti-proliferative, anti-migratory, and anti-invasive effects on cancer cells. To determine the role of sevoflurane on gastric cancer (GC) progression, we evaluated its effects on the proliferation, migration, and invasion of SGC7901, AGS, and MGC803 GC cells. Methods GC cells were exposed to different concentrations of sevoflurane (1.7, 3.4, or 5.1% v/v). Cell viability, migration, and invasion were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays. Immunohistochemical staining and immunoblotting were performed to analyze forkhead box protein 3 (FOXP3) protein expression in tissue specimens and cell lines, respectively. Results FOXP3 was downregulated in human GC specimens and cell lines. Functionally, FOXP3 overexpression significantly inhibited the proliferation, migration, and invasion of GC cells and accelerated their apoptosis. Moreover, sevoflurane significantly blocked GC cell migration and invasion compared with the findings in the control group. However, FOXP3 silencing neutralized sevoflurane-induced apoptosis and the inhibition of GC cell migration and invasion. Sevoflurane-induced apoptosis and the suppression of migration and invasion might be associated with FOXP3 overactivation in GC cells. Conclusions Sevoflurane activated FOXP3 and prevented GC progression via inhibiting cell migration and invasion in vitro.

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 IFT80 Improves Invasion Ability in Gastric Cancer Cell Line via ift80/p75NGFR/MMP9 Signaling

2018 ◽  
Vol 19 (11) ◽  
pp. 3616 ◽  
Author(s):  
Rui Wang ◽  
Xiaoyan Deng ◽  
Chengfu Yuan ◽  
Hongmei Xin ◽  
Geli Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Reverse Transcription ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Quantitative Reverse Transcription Pcr ◽  
Reverse Transcription Pcr ◽  
Gastric Cancer Cell Lines

The assembly and maintenance of cilia depend on intraflagellar transport (IFT) proteins, which play an important role in development and homeostasis. IFT80 is a newly defined IFT protein and partial mutation of IFT80 in humans causes diseases such as Jeune asphyxiating thoracic dystrophy (JATD) and short rib polydactyly (SRP) type III, both characterized by abnormal skeletal development. However, the role and mechanism of IFT80 in the invasion of gastric cancer is unknown. We established SGC-7901 and MKN-45 gastric cancer cell lines that stably overexpressed IFT80, as verified by quantitative reverse transcription-PCR, Western blot, and immunofluorescence. Matrix metalloproteinase-9 (MMP9) plays an important role in tumor invasion, and its expression was assessed by quantitative reverse transcription-PCR, Western blotting, and immunofluorescence. The invasion ability of IFT80 on SGC-7901 and MKN-45 cells was examined by the Matrigel invasion assay. The relationship between p75NGFR, and the p75NGFR antagonists, PD90780 and IFT80, were detected by quantitative reverse transcription-PCR and Western blotting. We first detected an IFT80 expression pattern, and found that IFT80 was highly expressed in gastric cancer clinical samples. Overexpression of IFT80 in the gastric cancer cell lines, SGC-7901 and MKN-45, led to lengthening cilia. Additionally, overexpression of IFT80 significantly improved proliferation and invasion, but inhibited apoptosis, in gastric cancer cells. We further found that overexpression of IFT80 increased p75NGFR and MMP9 mRNA and protein expression. Treatment with the p75NGFR antagonist PD90780 inhibited the increased invasion ability resulting from overexpression of IFT80 in SGC-7901 and MKN-45 gastric cancer cells. Thus, these results suggest that IFT80 plays an important role in invasion of gastric cancer through regulating the ift80/p75NGFR/MMP9 signal pathways.

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