Effects of Kinesin Family Member 23 on Biological Behavior of Gastric Cancer and the Mechanism

2021 ◽  
Vol 11 (9) ◽  
pp. 1655-1663
Author(s):  
Xuefeng Su ◽  
Junfeng Zheng
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Poor Prognosis ◽  
Biological Behavior ◽  
Mucosal Cell ◽  
Clinical Value ◽  
Cellular Mechanisms ◽  
Migration Ability ◽  
Invasion And Migration ◽  
The Impact

To clarify the impact of KIF23 on the biological behavior of gastric cancer (GC) and its clinical value in order to further explore the relevant molecular and cellular mechanisms of KIF23 in GC and find new biological targets for GC to provide relevant theoretical basis for the development of new antitumor drugs. Immunohistochemical technique was employed to identify the location and expression of KIF23 in GC and analyze the correlation between KIF23 and GC clinicopathological indexes. KIF23 abundance was preliminarily verified by normal gastric mucosal cell lines and various GC cell lines. Two KIF23 highly expressed GC cell lines were selected to elaborate the effect of KIF23 silencing on cell biological behaviors by siRNA interference. The influence of KIF23 on cell viability, proliferation and invasion were checked by MTT assay, cell colony formation experiments and transwell assay, respectively. GC cells and tissues both exhibited varying degrees of overexpression of KIF23 relative to normal gastric mucosal cells and paracancerous tissue, respectively. Elevated KIF23 level in GC was associated with poor prognosis and positively correlated with T,N, TNM stage and differentiation degree. Further, KIF23 silencing decreased cell proliferation, invasion and migration ability. KIF23 overexpression is found in GC cells and tissues and associated with poor prognosis. As oncogenes, KIF23 exerted crucial role in proliferation, invasion and cytokine secretion of GC cells.

KRAS mutation is associated with upregulation of integrin beta-4 expression leading to tumor invasion in colorectal cancer.

2019 ◽  
Vol 37 (4_suppl) ◽  
pp. 576-576
Author(s):  
Seo-Hyun Choi ◽  
Michael Marco ◽  
Ching-Tung Chen ◽  
Raphael Pelossof ◽  
Kevin Patrick O'Rourke ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Tumor Microenvironment ◽  
Cell Lines ◽  
Cell Invasion ◽  
Kras Mutation ◽  
Biological Behavior ◽  
Invasion And Migration ◽  
And Migration ◽  
The Impact

576 Background: KRAS mutation ( KRASmut) is associated with aggressive biological behavior and resistance to chemoradiotherapy in colorectal cancer (CRC). The tumor microenvironment is a critical component framing the biological behavior of cancers. We have recently shown that a KRASmut modulates the tumor microenvironment by reducing the expression of extracellular matrix (ECM) genes in CRC. The effect of a KRASmut on integrins, the epithelial cell receptors for ECM proteins, remains largely unknown. Here, we investigated the impact of KRASmut on integrin expression in CRC and the effect of integrin beta 4 (ITGB4) expression on CRC phenotype. Methods: The genomic profile of 79 locally advanced rectal cancers (LARC) was characterized by the MSK-IMPACT DNA assay and RNA sequencing by Hi-Seq platform. The transcriptomic changes associated with KRAS in the LARC cohort was validated in the TCGA colon cancer dataset. Expression of ITGB4 was investigated by immunofluorescence (IF) in 39 colon cancer specimens by counting ITGB4-positive cells in an E-cadherin positive epithelial population. The relationship between KRAS and ITGB4 was also explored by manipulating KRAS expression in human cell lines and genetically engineered mouse models (GEMMs). ITGB4 knockout in HCT116 CRC cell lines and organoids from GEMMs were generated with CRISPR/Cas9. ITGB4 expression was confirmed using qRT-PCR and western blotting. Cell proliferation was assessed with the MTT assay. Cell invasion and migration were assessed in a trans-well system. Results: ITGB4 gene expression was increased in KRASmut compared to KRASwildtype in LARC and TCGA. Increased ITGB4 expression in KRASmut colon cancers was also validated by IF (p = 0.0029). Introduction of KRASmut in HCT116 CRCs and GEMMs increased ITGB4 expression by 1.5 to 2 fold. Knockout of ITGB4 reduced the migration and invasion of HCT116 CRC cells but did not alter proliferation. Conclusions: KRASmutincreases the expression of ITGB4 in CRC. Increased ITGB4 expression is associated with CRC cell invasion and migration. These results inform the biology of tumor progression in KRASmut CRC tumors.

scholarly journals ANXA2 Silencing Inhibits Proliferation, Invasion, and Migration in Gastric Cancer Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Rui Xie ◽  
Jia Liu ◽  
Xuefeng Yu ◽  
Chunfeng Li ◽  
Yufeng Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
Invasion And Migration ◽  
Ags Cell Line ◽  
And Migration

Annexin A2 (ANXA2) has been well known to associate with the progress of malignant tumor. However, the biological behavior of ANXA2 in gastric cancer (GC) remains unclear. We made a hypothesis in transcriptome level from TCGA datasets. Then, we used immunohistochemical staining to quantify the expression level of ANXA2 protein in GC tissues compared with adjacent tissues. Quantitative real-time PCR and western blot were used for analyzing ANXA2 expression in human GC (SGC-7901, MKN-45, BGC-823, and AGS) cell lines. We investigated the effect of a lentivirus-mediated knock-down of ANXA2 on the proliferation, invasion and migration of gastric cancer AGS cells. Cell proliferation was examined by MTT and colony formation tests. Cell apoptosis and cycle were measured by flow cytometry. Migration and invasion were detected by transwell assay. We found that high expression of ANXA2 can increase the mobility of cancer cells from TCGA datasets. ANXA2 was upregulated in GC tissues compared with adjacent tissues. AGS cell line displayed significantly higher expression of ANXA2 among the four GC cell lines. In addition, ANXA2 silencing led to a weakened ability of proliferation, invasion, and migration in GC cells; targeting of ANXA2 may be a potential therapeutic strategy for GC patients.

scholarly journals miR-182-5p improves the viability, mitosis, migration, and invasion ability of human gastric cancer cells by down-regulating RAB27A

2017 ◽  
Vol 37 (3) ◽  
Author(s):  
Yuling Li ◽  
Shudong Chen ◽  
Zhengfei Shan ◽  
Liyan Bi ◽  
Shengqiang Yu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Migration Ability ◽  
Invasion And Migration ◽  
Gene Assay ◽  
And Migration

We investigated the effect of miR-182-5p on the viability, proliferation, invasion, and migration ability of human gastric cells by regulating the expression of RAB27A. Real-time PCR assay was used to detect the expression of miR-182-5 and RAB27A in human gastric carcinoma tissues, para-carcinoma tissues, and different cell lines. Western blotting was also used to determine the RAB27A expression in both tissues and cell lines. We chose the HGC-27 cell line as experiment subject as it demonstrated the highest miR-182-5p level. HGC-27 cells were transfected with different vectors and the cell viability, mitosis, invasion, and migration ability were measured through MTT assay, flow cytometry (FCM) analysis, Transwell assay, and wound healing assay. In comparison with the normal tissues, miR-182-5p is expressed at a higher level in gastric cancer (GC) tissues, while RAB27A is expressed at a lower level in cancerous tissues. The down-regulation of miR-182-5p and up-regulation of RAB27A can significantly decrease the viability, migration, invasion, and mitosis of HGC-27 cells. The target relationship between miR-182-5p and RAb27A was confirmed through a dual-luciferase reporter gene assay and Western blot assay. miR-182-5p enhances the viability, mitosis, migration, and invasion of human GC cells by down-regulating RAB27A.

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.

LncRNA PCAT18/miR-301a/TP53INP1 axis is involved in gastric cancer cell viability, migration and invasion

2020 ◽  
Vol 168 (5) ◽  
pp. 547-555
Author(s):  
Jin Dou ◽  
Daoyuan Tu ◽  
Haijian Zhao ◽  
Xiaoyu Zhang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Cell Lines ◽  
Underlying Mechanism ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Proliferation And Metastasis ◽  
And Migration ◽  
Cell Proliferation And Metastasis

Abstract MiR-301a is as an oncogene involved in the regulation of gastric cancer (GC) progression, but the underlying mechanism is unclear. This study was to explore the lncRNA PCAT18/miR-301a/TP53INP1 axis in regulating the GC cell proliferation and metastasis. In the present study, GC tissues and cell lines were collected for the detection of PCAT18 expression. Herein, we found that PCAT18 is significantly decreases in human GC tissues and five GC cell lines. Overexpression of PCAT18 inhibits cell viability, invasion and migration of GC cells and tumour growth of GC xenograft tumours. PCAT18 negatively regulates the expression level of miR-301a. The interaction between PCAT18 and miR-301a is confirmed by RIP and RNA pull down. MiR-301a mimic increases cell viability and promotes cell migration and invasion and reverses the inhibitory action of PCAT18. TP53INP1 expression is negatively regulated by miR-301a and TP53INP1/miR-301a is involved in GC viability, migration and invasion. The promoting of PCAT18 on TP53INP1 expression is abolished by miR-301a overexpression. In conclusion, lncRNA PCAT18 acts as a tumour suppressor for GC and lncRNA PCAT18, miR-301a and TP53INP1 comprise a signal axis in regulating GC cell proliferation, migration and invasion.

scholarly journals Role of ADP Ribosylation Factor Guanylate Kinase 1 in the Malignant Biological Behavior of Gastric Cancer

2021 ◽  
Author(s):  
Qiong Luo ◽  
Suyun Zhang ◽  
Fan Yang ◽  
Rui Feng ◽  
Qian Xu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Nude Mice ◽  
Caspase 3 ◽  
Cell Counting ◽  
Biological Behavior ◽  
Guanylate Kinase ◽  
Invasion And Migration ◽  
Adp Ribosylation ◽  
And Migration ◽  
Adp Ribosylation Factor

Abstract Objectives: To study the effects of ADP ribosylation factor guanylate kinase 1 gene (ASAP1) on the biological behavior of malignant gastric cancer (GC), and explore its possible molecular mechanisms in tumorigenesis and tumor progression.Methods: Quantitative PCR and western blotting (WB) were performed to measure ASAP1 mRNA and protein expression in the GES-1 epithelial cell line, which is derived from normal human mucosa, and three GC cell lines. Molecular biology techniques such as lentivirus packaging, infection, and screening were used to obtain BGC823 GC cells overexpressing ASAP1 and BGC823 and MKN45 cells with ASAP1 knocked down. The Cell Counting Kit-8 assay, colony formation assay, flow cytometry using Annexin V/propidium iodide, Transwell migration and invasion assays, and scratch assay were used to assess the malignant biological behavior of GC cells with ASAP1 overexpression and knockdown. WB was conducted to evaluate the effects of ASAP1 expression on angiogenesis, as well as on the expression of matrix metalloproteinases (MMPs), apoptotic proteins, and epithelial-mesenchymal transition (EMT)-related proteins. Nude mice bearing transplanted tumors were evaluated to determine the effect of ASAP1 knockdown on BGC823 GC cells.Results: ASAP1 expression in GC cells was greater than that in GES-1 normal gastric mucosal epithelial cells. ASAP1 overexpression significantly enhanced the proliferation, invasion, and migration of GC cells and reduced apoptosis; whereas ASAP1 knockdown significantly reduced the proliferation, invasion, and migration of GC cells and promoted apoptosis. In the ASAP1-knockdown group, expression of cleaved-caspase 3, cleaved-poly-ADP-ribose polymerase (PARP), and the epithelial marker E-cadherin increased significantly, whereas the expression of MMP2, MMP9, vascular endothelial growth factor A (VEGFA), and the mesenchymal markers N-cadherin, and vimentin decreased significantly (P<0.01). Knockdown of ASAP1 inhibited the growth of subcutaneously implanted tumors in nude mice.Conclusions: ASAP1 overexpression strongly promotes—whereas knockdown of ASAP1 effectively weakens—the malignant biological behavior of GC cells, possibly by reducing VEGFA expression and thus reducing angiogenesis, upregulating the expression of cleaved-caspase 3 and cleaved-PARP, and reducing the activity of MMPs and EMT.

scholarly journals Relationship between microRNA-27a and efficacy of neoadjuvant chemotherapy in gastric cancer and its mechanism in gastric cancer cell growth and metastasis

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Chunlei Xu ◽  
Hong Cheng ◽  
Na Li ◽  
Ning Zhou ◽  
Xushan Tang
Keyword(s):  
Gastric Cancer ◽  
Neoadjuvant Chemotherapy ◽  
Cell Line ◽  
Proliferation Rate ◽  
Clinical Value ◽  
Cancer Cell Growth ◽  
Invasion And Migration ◽  
Mrna And Protein Expression ◽  
Mucosa Cell ◽  
And Migration

Abstract Objective: The aim of the present study is to investigate the relationship between microRNA-27a (miR-27a) and the efficacy of neoadjuvant chemotherapy in gastric cancer (GC) and its mechanism in the growth and metastasis of GC cells. Methods: The expression of miR-27a in serum of 74 GC patients received neoadjuvant chemotherapy was detected by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Clinical value and prognosis of miR-27a expression in predicting the efficacy of neoadjuvant chemotherapy in GC were evaluated. Besides, GC cells with low miR-27a expression were transfected with miR-27a mimics, and cells with high miR-27a expression were transfected with miR-27a inhibitors and secreted frizzled-related protein 1 (SFRP1) siRNA. A series of experiments were applied for the determination of cell viability, invasion and migration of GC cells. Results: After neoadjuvant chemotherapy, the expression of miR-27a in serum of GC patients decreased significantly. Additionally, the expression of miR-27a in GC cell line was significantly higher than that in normal gastric mucosa cell line. Meanwhile, after down-regulating the expression of miR-27a in GC cells, the mRNA and protein expression of SFRP1 increased, the proliferation rate of cells slowed down, and the ability of invasion and migration decreased. Furthermore, combined with low expression of miR-27a and SFRP1, the proliferation rate of GC cells increased and the ability of invasion and migration increased. Conclusion: Collectively, our study highlights that the high expression of miR-27a indicates the poor efficacy and prognosis of neoadjuvant chemotherapy in GC patients. Down-regulation of miR-27a can inhibit the growth and metastasis of GC cells via up-regulation of SFRP1.

The Mechanism of Human Umbilical Mesenchymal Stem Cells (HUMSC) on Biological Behavior of Human Papillomavirus (HPV) Cells Through Restraining the Programmed Cell Death Protein 1/Programmed Cell Death Ligand 1 (PD-1/PD-L1) Signal Pathway

2022 ◽  
Vol 12 (2) ◽  
pp. 265-272
Author(s):  
Min Wang ◽  
Yanong Zhu ◽  
Tongmin Li ◽  
Chaofeng Xia
Keyword(s):  
Cell Death ◽  
Test Group ◽  
Signal Pathway ◽  
Biological Behavior ◽  
Control Group ◽  
Migration Ability ◽  
Blank Group ◽  
Invasion And Migration ◽  
And Migration

Biological behavior of HPV cell was observed by HUMSC through restraining PD-1/PD-L1 signal pathway. And HUMSC was adopted as target cell for the treatment on HPV. The rat HPV model was established and divided into three groups including blank group, control group and test group according to different reagents being injected into rats. Use HE staining method to observe the cancerous transformation of tumor tissue sections. The gene presentation of PD-1/PD-L1 and lymphocyte was detected with Western blot. The invasion and migration condition of cancer cells was observed from experiment in vitro. The quantity of cancer cells in test group was the least. And invasion and migration ability in test group was the weakest. The control group was the second. The number of tumor cells in the blank group was the largest. Strongest ability to invade and migrate. The presentation of PD-L1 was restrained partly by HUMSC. The increasing of immune-associated cells could be prompted by HUMSC. The quantity of CD3+, CD4+ and CD8+ in PB was the most in test group. The expression of blank groups is the lowest than others restrained by HUMSC. And quantity of abundant immune cells including CD3+, CD4+ and CD8+ could be activated partly through activating immune action of body. And monitoring function of immune system on HPV cells could be increased effectively. The invasion and migration ability in vitro of HPV could be reduced partly.

scholarly journals Upregulation of musashi1 increases malignancy of hepatocellular carcinoma via the Wnt/β-catenin signaling pathway and predicts a poor prognosis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Qiuhua Liu ◽  
Cuijie Zhou ◽  
Bo Zhang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Poor Prognosis ◽  
Liver Tumors ◽  
Clinicopathological Characteristics ◽  
Invasion And Migration ◽  
Potential Biomarker ◽  
Hcc Cells

Abstract Background Hepatocellular carcinoma (HCC) is a common human malignant cancer due to a high metastatic capacity and the recurrence rate is also high. This study is aim to investigate the role of musashi1 as a potential biomarker for therapy of HCC. Methods The mRNA and protein expression levels of musashi1 were detected in HCC samples and cell lines. The malignant properties of HCC cells, including proliferation, invasion and migration were measured by overexpressing or knocking down expression of musashi1. Additionally, the correlation between musashi1 and clinicopathological indexes and prognosis were analyzed. The expression of CD44 was measured and the correlation between CD44 and musashi1 was analyzed. Results In vitro cytological experiments demonstrated that musashi1 was elevated in HCC samples and cell lines and this increased expression affected cancer cell viability, migration and invasive capacity by activating of the Wnt/β-catenin signaling pathway. Analysis of clinicopathological characteristics suggested that up-regulation of musashi1 was related to metastasis potential and a poor prognosis. Besides, there was a positive correlation between CD44 and musashi1 expression. Upregulation of musashi1 in malignant liver tumors may have contributed to the maintenance of stem-cell like characteristics of HCC cells. Conclusions Upregulation of musashi1 could enhance malignant development of HCC cells and thus might be a novel marker for HCC therapy.

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