scholarly journals Arsenic sulfide inhibits cell migration and invasion of gastric cancer in vitro and in vivo

2015 ◽  
pp. 5579 ◽  
Author(s):  
Siyu Chen ◽  
Lian Zhang ◽  
Sungkyoung Kim ◽  
Wenping Ding ◽  
Yingying Tong ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Migration And Invasion ◽  
Arsenic Sulfide ◽  
Cell Migration And Invasion

scholarly journals FOXF2-Mediated lncRNA LINC02532 Promotes Gastric Cancer Cell Migration and Invasion By Decreasing SOX7 mRNA Stability

2021 ◽  
Author(s):  
Cheng Zhang ◽  
Chun-Dong Zhang ◽  
Jun-Peng Pei ◽  
Yong-Zhi Li ◽  
Maimaititusun Yusupu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Transcriptional Regulation ◽  
Cell Migration ◽  
Mrna Stability ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion

Abstract Background LncRNAs are known to play a crucial role in the initiation and progression of human diseases, especially cancers. Our previous study demonstrated that dysregulation of LINC02532 facilitated the malignant phenotype of gastric cancer (GC). However, the potential molecular mechanisms regarding the upstream and downstream regulation of LINC02532 in GC progression remain unclear. Methods RNA-Seq and clinical data from public databases were used for gene expression and clinical analyses. The subcellular location of LINC02532 was predicted by the bioinformatics tools and further validated by the RNA-Fluorescence in situ hybridization (FISH) assay. The effect of FOXF2/LINC02532/SOX7 axis in GC cell migration and invasion was evaluated using in vitro and in vivo assays. The transcriptional regulation role of FOXF2 and the mRNA stability of SOX7 were explored by dual-luciferase reporter assay and Actinomycin-D drug assay. Results We found that high LINC02532 expression was associated with poor prognosis of GC. Furthermore, a Cox regression model indicated that LINC02532 was an independent prognostic factor for GC patients. Using in vitro and in vivo assays, we found that LINC02532 promoted GC cell migration and invasion, as well as tumour growth and metastasis in nude mice. Mechanistically, LINC02532 decreased SOX7 mRNA stability by binding to its 3’UTR, resulting in reduced SOX7 expression. In addition, FOXF2 was identified as a transcriptional factor of LINC02532 and was shown to repress LINC02532 expression by negative transcriptional regulation. Conclusions Together, these findings show that LINC02532 promotes GC progression through epithelial–mesenchymal transition (EMT). Cross-talk between the FOXF2/LINC02532/SOX7 axis may provide a novel target for the treatment and prognostic prediction of GC.

scholarly journals LIMK1 promotes peritoneal metastasis of gastric cancer and is a therapeutic target

Oncogene ◽  
2021 ◽  
Author(s):  
Xi Kang ◽  
Weilin Li ◽  
Weixin Liu ◽  
Han Liang ◽  
Jingyu Deng ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Peritoneal Metastasis ◽  
Therapeutic Target ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
Cell Migration And Invasion

AbstractPeritoneal metastasis is a common form of metastasis among advanced gastric cancer patients. In this study, we reported the identification of LIM domain kinase 1 (LIMK1) as a promoter of gastric cancer peritoneal metastasis, and its potential to be a therapeutic target of dabrafenib (DAB). Using transcriptomic sequencing of paired gastric cancer peritoneal metastasis, primary tumors, and normal gastric tissues, we first unveiled that LIMK1 is selectively up-regulated in metastatic tumors. Increased LIMK1 in gastric cancer peritoneal metastasis was validated by immunohistochemistry analysis of an independent patient cohort. In vitro functional studies demonstrated that LIMK1 knockout or knockdown significantly inhibited cell migration and invasion of gastric cancer cells. LIMK1 knockout also abrogated peritoneal and liver metastases of gastric cancer cells in nude mice in vivo. Dabrafenib, a small molecule targeting LIMK1, was found to decrease cell migration and invasion of gastric cancer cells in vitro and abolish peritoneal and liver metastasis formation in vivo. Mechanistically, either LIMK1 knockout or Dabrafenib inhibited LIMK1 expression and phosphorylation of its downstream target cofilin. Taken together, our results demonstrated that LIMK1 functions as a metastasis promoter in gastric cancer by inhibiting LIMK1-p-cofilin and that Dabrafenib has the potential to serve as a novel treatment for gastric cancer peritoneal metastasis.

scholarly journals Downregulation of long noncoding RNA LINC01419 inhibits cell migration, invasion, and tumor growth and promotes autophagy via inactivation of the PI3K/Akt1/mTOR pathway in gastric cancer

2019 ◽  
Vol 11 ◽  
pp. 175883591987465 ◽  
Author(s):  
Lin-Lin Wang ◽  
Lei Zhang ◽  
Xiao-Feng Cui
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Tumor Growth ◽  
Noncoding Rna ◽  
Mtor Pathway ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Tumor Growth And Metastasis

Background: Accumulating evidence has highlighted the crucial role of long noncoding RNAs (lncRNAs) in the tumorigenesis of gastric cancer (GC), which is the most common gastrointestinal malignancy. The present study aimed to identify the capacity of lncRNA LINC01419 (LINC01419) in GC progression, with the potential mechanism explored. Methods: Highly expressed lncRNAs were identified by in silico analysis, with the LINC01419 expression in GC tissues measured using reverse transcription-quantitative PCR (RT-qPCR). The GC cells were subsequently transfected with siRNA against LINC01419 or Rapamycin (the inhibitor of the mTOR pathway), or both, in order to measure cell migration and invasion in vitro as well as tumor growth and metastasis in vivo. Moreover, the expression of PI3K/Akt1/mTOR pathway-associated factors was determined. Results: LINC01419, highly expressed in GC samples of the Gene Expression Omnibus database, was observed to be markedly upregulated in GC tissues. Moreover, LINC01419 silencing, or PI3K/Akt1/mTOR pathway inhibition, exhibited an inhibitory role in GC cell migration and invasion in vitro, coupled with promoted cell autophagy in vitro, and inhibited tumor growth and metastasis in vivo. It was also revealed that LINC01419 silencing blocked the PI3K/Akt1/mTOR pathway, as proved by decreased extents of Akt1 and mTOR phosphorylation. Conclusions: In conclusion, LINC01419 inhibition may suppress GC cell invasion and migration, and promote autophagy via inhibition of the PI3K/Akt1/mTOR pathway. This provides significant theoretical basis and possibilities for further elucidation of the molecular mechanism of GC and finding new molecular-targeted therapeutic regimens.

scholarly journals Resveratrol Enhances Inhibition Effects of Cisplatin on Cell Migration and Invasion and Tumor Growth in Breast Cancer MDA-MB-231 Cell Models In Vivo and In Vitro

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2204
Author(s):  
Meng-Die Yang ◽  
Yang Sun ◽  
Wen-Jun Zhou ◽  
Xiao-Zheng Xie ◽  
Qian-Mei Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Tumor Growth ◽  
Cell Viability ◽  
Synergistic Effects ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Tgf Β1

Triple-negative breast cancer (TNBC) is a refractory type of breast cancer that does not yet have clinically effective drugs. The aim of this study is to investigate the synergistic effects and mechanisms of resveratrol combined with cisplatin on human breast cancer MDA-MB-231 (MDA231) cell viability, migration, and invasion in vivo and in vitro. In vitro, MTS assays showed that resveratrol combined with cisplatin inhibits cell viability as a concentration-dependent manner, and produced synergistic effects (CI < 1). Transwell assay showed that the combined treatment inhibits TGF-β1-induced cell migration and invasion. Immunofluorescence assays confirmed that resveratrol upregulated E-cadherin expression and downregulated vimentin expression. Western blot assay demonstrated that resveratrol combined with cisplatin significantly reduced the expression of fibronectin, vimentin, P-AKT, P-PI3K, P-JNK, P-ERK, Sma2, and Smad3 induced by TGF-β1 (p < 0.05), and increased the expression of E-cadherin (p < 0.05), respectively. In vivo, resveratrol enhanced tumor growth inhibition and reduced body weight loss and kidney function impairment by cisplatin in MDA231 xenografts, and significantly reduced the expressions of P-AKT, P-PI3K, Smad2, Smad3, P-JNK, P-ERK, and NF-κB in tumor tissues (p < 0.05). These results indicated that resveratrol combined with cisplatin inhibits the viability of breast cancer MDA231 cells synergistically, and inhibits MDA231 cells invasion and migration through Epithelial-mesenchymal transition (EMT) approach, and resveratrol enhanced anti-tumor effect and reduced side of cisplatin in MDA231 xenografts. The mechanism may be involved in the regulations of PI3K/AKT, JNK, ERK and NF-κB expressions.

scholarly journals A high-throughput 3D bioprinted cancer cell migration and invasion model with versatile and broad biological applicability

2021 ◽  
Author(s):  
MoonSun Jung ◽  
Joanna Skhinas ◽  
Eric Y Du ◽  
Maria Kristine Tolentino ◽  
Robert Utama ◽  
...  
Keyword(s):  
Cell Migration ◽  
High Throughput ◽  
Drug Screening ◽  
Cancer Biology ◽  
Cell Movement ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Drop On Demand

Understanding the underlying mechanisms of migration and metastasis is a key focus of cancer research. There is an urgent need to develop in vitro 3D tumor models that can mimic physiological cell-cell and cell-extracellular matrix interactions, with high reproducibility and that are suitable for high throughput (HTP) drug screening. Here, we developed a HTP 3D bioprinted migration model using a bespoke drop-on-demand bioprinting platform. This HTP platform coupled with tunable hydrogel systems enables (i) the rapid encapsulation of cancer cells within in vivo tumor mimicking matrices, (ii) in situ and real-time measurement of cell movement, (iii) detailed molecular analysis for the study of mechanisms underlying cell migration and invasion, and (iv) the identification of novel therapeutic options. This work demonstrates that this HTP 3D bioprinted cell migration platform has broad applications across quantitative cell and cancer biology as well as drug screening.

The role of STEAP1 in the biological behavior of gastric cancer

2020 ◽  
Author(s):  
Zhe Zhang ◽  
Wen-bin Hou ◽  
Chao Zhang ◽  
Dong-dong Zhang ◽  
Wen An ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Protein Expression ◽  
Signaling Pathways ◽  
Rna Sequencing ◽  
Migration And Invasion ◽  
Cell Migration And Invasion

Abstract Background: Six-transmembrane epithelial antigen 1 (STEAP1) is associated with the occurrence and development of cancer. This study aimed to clarify the role of STEAP1 in gastric cancer tumor growth and metastasis, as well as its molecular mechanism of action.Methods: Statistical methods were used for clinical data analysis. Protein expression was detected using immunohistochemistry. The mRNA and protein expression in the cell cultures were detected using reverse transcription-polymerase chain reaction and western blot analysis. Overexpression and silencing models were constructed using plasmid and lentivirus transfection. To detect cell proliferation in vitro, Cell Counting Kit-8, flow cytometry, and colony formation assays were used; transwell and wound healing assays were used to detect cell migration and invasion; RNA sequencing was used for identifying differentially expressed genes; ELISA assay was used to detect the secretory proteins in cells. For in vivo experiments, nude BALB/c mice were used for detecting subcutaneous tumorigenesis and intraperitoneal implantation.Results: STEAP1 was overexpressed in gastric cancer tissues and cell lines. Single factor and Cox analyses showed that STEAP1 gene expression level correlated with poor prognosis. Upregulation of STEAP1 increased cell proliferation, migration, and invasion, which decreased after STEAP1 was knocked down. These changes were achieved via the activation of the AKT/FoxO1 pathway and epithelial-mesenchymal transformation (EMT). The RNA sequencing results indicated that STEAP1 was closely related to inflammatory reactions. STEAP1 can regulate the inflammation-related molecules, IL-1β and IL-6, via the NF-kB and ERK/c-Jun signaling pathways. The in vivo animal experiments showed that STEAP1 knock down, resulted in a decrease in the subcutaneous tumor and peritoneal tumor formation.Conclusion: STEAP1 was overexpressed in gastric cancer and closely associated with OS. STEAP1 can regulate the cell cycle via the Akt/FoxO1 pathway to influence cell proliferation. STEAP1 may affect cell migration and invasion via EMT action. In addition, STEAP1 may mediate the inflammatory response by regulating IL1β and IL6 via the NF-kB and the ERK/c-Jun signaling pathways.

Gold(III) porphyrin 1a inhibited nasopharyngeal carcinoma metastasis in vivo and inhibited cell migration and invasion in vitro

2010 ◽  
Vol 294 (2) ◽  
pp. 159-166 ◽  
Author(s):  
Ching Tung Lum ◽  
Xiong Liu ◽  
Raymond Wai-Yin Sun ◽  
Xiang-Ping Li ◽  
Ying Peng ◽  
...  
Keyword(s):  
Cell Migration ◽  
Nasopharyngeal Carcinoma ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Carcinoma Metastasis

scholarly journals RANK promotes colorectal cancer migration and invasion by activating the Ca2+-calcineurin/NFATC1-ACP5 axis

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Qian Liang ◽  
Yun Wang ◽  
Yingsi Lu ◽  
Qingqing Zhu ◽  
Wenlin Xie ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Nuclear Translocation ◽  
Migration And Invasion ◽  
Tartrate Resistant Acid Phosphatase ◽  
Activated T Cells ◽  
Cell Migration And Invasion ◽  
Cell Metastasis

AbstractThe tumor necrosis factor (TNF) receptor superfamily member 11a (TNFRSF11a, also known as RANK) was demonstrated to play an important role in tumor metastasis. However, the specific function of RANK in colorectal cancer (CRC) metastasis and the underlying mechanism are unknown. In this study, we found that RANK expression was markedly upregulated in CRC tissues compared with that in matched noncancerous tissues. Increased RANK expression correlated positively with metastasis, higher TNM stage, and worse prognosis in patients with CRC. Overexpression of RANK promoted CRC cell metastasis in vitro and in vivo, while knockdown of RANK decreased cell migration and invasion. Mechanistically, RANK overexpression significantly upregulated the expression of tartrate-resistant acid phosphatase 5 (TRAP/ACP5) in CRC cells. Silencing of ACP5 in RANK-overexpressing CRC cells attenuated RANK-induced migration and invasion, whereas overexpression of ACP5 increased the migration and invasion of RANK-silencing cells. The ACP5 expression was transcriptionally regulated by calcineurin/nuclear factor of activated T cells c1 (NFATC1) axis. The inhibition of calcineurin/NFATC1 significantly decreased ACP5 expression, and attenuated RANK-induced cell migration and invasion. Furthermore, RANK induced phospholipase C-gamma (PLCγ)-mediated inositol-1,4,5-trisphosphate receptor (IP3R) axis and stromal interaction molecule 1 (STIM1) to evoke calcium (Ca2+) oscillation. The RANK-mediated intracellular Ca2+ mobilization stimulated calcineurin to dephosphorylate NFATC1 and induce NFATC1 nuclear translocation. Both blockage of PLCγ-IP3R axis and STIM1 rescued RANK-induced NFATC1 nuclear translocation, ACP5 expression, and cell metastasis. Our study revealed the functional expression of RANK in human CRC cells and demonstrated that RANK induced the Ca2+-calcineurin/NFATC1-ACP5 axis in the regulation of CRC metastasis, that might be amenable to therapeutic targeting.

scholarly journals A Research of STEAP1 on the Biological Behavior of Gastric Cancer

2020 ◽  
Author(s):  
Zhe Zhang ◽  
Huimian Xu
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Protein Expression ◽  
Cell Counting ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Mesenchymal Transformation

Abstract Introduction:Six-Transmembrane Epithelial Antigene of the Prostate 1 (STEAP1) is associated with the occurrence and development of cancer. This study aimed to clarify the role of STEAP1 in gastric cancer tumor growth and metastasis, as well as its molecular mechanism of action. Methods：Statistical methods were used for clinical data analysis. Protein expression was detected using immunohistochemistry(IHC). The mRNA and protein expression in the cell cultures were detected using reverse transcription-polymerase chain reaction(RT-PCR) and western blot analysis. Overexpression and silencing models were constructed using plasmid and lentivirus transfection. To detect cell proliferation in vitro, Cell Counting Kit-8(CCK-8), flow cytometry, and colony formation assays were used; transwell and wound healing assays were used to detect cell migration and invasion; For in vivo experiments, nude BALB/c mice were used for detecting subcutaneous tumorigenesis and intraperitoneal implantation. Results：We found STEAP1 was overexpressed in gastric cancer tissues and cell lines. Single factor and Cox analyses showed that STEAP1 gene expression level correlated with poor prognosis. Upregulation of STEAP1 increased cell proliferation, migration, and invasion, which decreased after STEAP1 was knocked down. These changes were achieved via the activation of the AKT/FoxO1 pathway and epithelial-mesenchymal transformation (EMT). The in vivo animal experiments showed that STEAP1 knock down, resulted in a decrease in the subcutaneous tumor and peritoneal tumor formation.Conclusions：STEAP1 was overexpressed in gastric cancer and closely connected with OS. STEAP1 can regulate the cell cycle via the Akt/FoxO1 pathway to influence cell proliferation. STEAP1 may affect cell migration and invasion via EMT induction.

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