scholarly journals NDRG1 Inhibition of Tumor Progression in Caco2 Cells

2021 ◽  
Author(s):  
Yixiao He ◽  
Yuzhu Ji ◽  
Hairong Hua ◽  
Yu Zhu ◽  
Peng Yu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Tumor Progression ◽  
Early Stage ◽  
Strong Relationship ◽  
S Phase ◽  
Cell Counting ◽  
Invasion And Migration ◽  
Caco2 Cells ◽  
And Migration

Abstract Background: Colorectal cancer (CRC) is a leading cause of cancer death worldwide. Invasiveness and migration are the main cause of death, and so there is a need to find a sensitive, reliable molecular marker that can predict the migration of colorectal cancer at an early stage. NDRG1 (N-myc Downstream Regulated Gene 1) has been reported to be a multifunctional gene that has a strong relationship with tumor invasion and migration, but theories about the current role of NDRG1 in colorectal cancer remains to be conclusively determined. Methods and Results: Through lentivirus infection and CRISPR/Cas9 methods, respectively, we established that NDRG1 stably overexpressed and knocked out Caco2 cell lines. CCK8(Cell Counting kit 8) data showed that NDRG1 inhibited Caco2 proliferation. Flow cytometry further confirmed that the cell cycle can be arrested at the G1/S phase when NDRG1 overexpresses, while the number of G2 phase cells significantly increased after NDRG1 was knocked out. This means that NDRG1 inhibited the proliferation of Caco2 cells by arresting the cell cycle in the G1/S phase. Our data also demonstrated that NDRG1 promotes early cell apoptosis. The strength of invasion and migration was decreased when NDRG1 overexpressed. Conclusions: Our results underline that NDRG1 inhibits tumor progression in Caco2 cells. These findings may provide a new potential therapeutic strategy for the treatment of CRC.

Nobiletin Inhibits Proliferation, Invasion, Migration and Angiogenesis in Colorectal Cancer Cells

2019 ◽  
Vol 9 (5) ◽  
pp. 662-667
Author(s):  
Jing Li ◽  
Zaijun Li ◽  
Fei Zheng
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Invasion ◽  
Human Cancer ◽  
Cell Counting ◽  
Control Group ◽  
Dependent Manner ◽  
Invasion And Migration ◽  
Traditional Chinese Herbal Medicine ◽  
And Migration

Aim/Background: The nobiletin is a polymethoxyflavonoid isolated from citrus, which is a traditional Chinese herbal medicine. The nobiletin could inhibit the development of human cancer. However, the role of nobiletin in human colorectal cancer (CRC) remains unknown. The present study aimed to explore the nobiletin function in CRC cell proliferation, migration, invasion and angiogenesis as well as the occurrence mechanisms. Methods: The cell counting kit-8 assay (CCK-8 assay) and Brdu (5-brom-2-odeoxyuridine) staining assay were used to determine the effect of nobiletin on cell proliferation. The transwell assay and wound healing assay were used to assess cell invasion and migration. The western blot analysis was performed to determine the expression of VEGFA, Ang2, p65, p-p65, STAT3, p-STAT3 in CRC cell. Result: Compared with the control group (0 mg/L), the cell proliferation was increased in a dose-dependent manner with 10, 50, 100, 150 mg/L nobiletin for 48 h. The nobiletin inhibited cell invasion and migration and suppressed the expression of VEGFA and Ang2 to block angiogenesis in the colorectal cancer. In addition, we found that nobiletin inhibited cell proliferation, invasion, migration and angiogenesis by suppression of NF-κB/STAT3 pathway. Conclusion: The study provided evidence that nobiletin inhibited cell proliferation, invasion, migration and angiogenesis in the colorectal cancer.

scholarly journals Role of B7-H4 siRNA in Proliferation, Migration, and Invasion of LOVO Colorectal Carcinoma Cell Line

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Hai-xia Peng ◽  
Wei-qi Wu ◽  
Da-ming Yang ◽  
Rong Jing ◽  
Ji Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Colorectal Carcinoma ◽  
Cxcr4 Expression ◽  
Gene Set Enrichment Analysis ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Stat3 Phosphorylation ◽  
Lovo Cells ◽  
And Migration

Objectives. Colorectal cancer is one of the most common malignancies. Recent studies investigated that B7-H4 is highly expressed in various cancers. We aimed at exploring the effect of B7-H4 siRNA on proliferation, invasion, and migration of LOVO cells which expressed B7-H4 notably.Design and Methods. Colon adenocarcinoma dataset was downloaded from The Cancer Genome Atlas. 35 colorectal cancer patients admitted to Shanghai Tongren Hospital were enrolled in this study. Cell proliferation and cell cycle distribution were identified by CCK8 and flow cytometry, respectively. Transwell assay was performed to detect the invasion and migration of LOVO cells. CXCL12/CXCR4 expression and JAK2/STAT3 phosphorylation were determined by real-time PCR and western blot.Results. B7-H4 expressed is elevated in colorectal cancer tissues than in the adjacent normal tissues. B7-H4 siRNA effectively inhibited the proliferation at 24 h and 48 h, arrested cell cycle at G0/G1, and suppressed cell invasion and migration. Gene set enrichment analysis showed that CXCL12/CXCR4 and JAK/STAT were correlative with the B7-H4 expression. Additionally, CXCL12/CXCR4 expression and JAK2/STAT3 phosphorylation were reduced.Conclusions. B7-H4 siRNA can effectively inhibit proliferation, invasion, and migration of LOVO cells by targeting CXCL12/CXCR4 and JAK2/STAT3 signaling, which can serve as a new target for colorectal carcinoma treatment.

scholarly journals HSPA4 knockdown retarded progression and development of colorectal cancer

2020 ◽  
Author(s):  
Mingliang Zhang ◽  
Weigang Dai ◽  
Zhanyu Li ◽  
Liang Tang ◽  
Jianhui Chen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Molecular Mechanisms ◽  
Apoptotic Cell ◽  
Molecular Therapy ◽  
Cell Counting ◽  
Antibody Array ◽  
And Migration

Abstract Background: Colorectal cancer (CRC) is the third most common cancer worldwide and the fourth most common cause of cancer death. The heat shock 70kDa protein 4 (HSPA4) participate in progression and development of cancers. However, the cellular functions, potential molecular mechanisms of HSPA4 in CRC are still largely unknown. Methods: In this study, qRT-PCR and Western Blot were used to identify the constructed HSPA4 knockdown cell lines, which was further used to construct mouse xenotransplantation models. Effects of HSPA4 knockdown on cell proliferation, apoptotic, cell cycle and migration of CRC were examined using Celigo cell counting assay, Flow cytometry, wound healing assay and Transwell assay, respectively. In addition, Human Apoptosis Antibody Array was performed to explore downstream molecular mechanism of HSPA4 in CRC cells. Results: HSPA4 was overexpressed in CRC, which was positively associated with lymphatic metastasis (N value), number of Lymph node. In addition, high expression of HSPA4 predicted poor prognosis of patients with CRC. Furthermore, HSPA4 knockdown inhibit proliferation, migration, promote apoptosis, and arrest cell cycle of CRC cells in vitro. Moreover, in vivo results supported HSPA4 knockdown inhibit tumor growth. Additionally, the induction of apoptosis of CRC cells by HSPA4 knockdown required the participation of a series of apoptosis-related proteins. The downregulation of HSPA4 promoted the progression of CRC cells, which resulted in alterations of PI3K/Akt, CCND1 and CDK6 in downstream signaling pathways. Conclusions: In sum, the downregulation of HSPA4 promoted CRC and may be a potential target for molecular therapy.

scholarly journals Hspa4 Knockdown Retarded Progression and Development of Colorectal Cancer

2020 ◽  
Author(s):  
Mingliang Zhang ◽  
Weigang Dai ◽  
Zhanyu Li ◽  
Liang Tang ◽  
Jianhui Chen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Molecular Mechanisms ◽  
Apoptotic Cell ◽  
Molecular Therapy ◽  
Cell Counting ◽  
Antibody Array ◽  
And Migration

Abstract Background Colorectal cancer (CRC) is the third most common cancer worldwide and the fourth most common cause of cancer death. The heat shock 70 kDa protein 4 (HSPA4) participate in progression and development of cancers. However, the cellular functions, potential molecular mechanisms of HSPA4 in CRC are still largely unknown. Methods In this study, qRT-PCR and Western Blot were used to identify the constructed HSPA4 knockdown cell lines, which was further used to construct mouse xenotransplantation models. Effects of HSPA4 knockdown on cell proliferation, apoptotic, cell cycle and migration of CRC were examined using Celigo cell counting assay, Flow cytometry, wound healing assay and Transwell assay, respectively. In addition, Human Apoptosis Antibody Array was performed to explore downstream molecular mechanism of HSPA4 in CRC cells. Results HSPA4 was overexpressed in CRC, which was positively associated with lymphatic metastasis (N value), number of Lymph node. In addition, high expression of HSPA4 predicted poor prognosis of patients with CRC. Furthermore, HSPA4 knockdown inhibit proliferation, migration, promote apoptosis, and arrest cell cycle of CRC cells in vitro. Moreover, in vivo results supported HSPA4 knockdown inhibit tumor growth. Additionally, the induction of apoptosis of CRC cells by HSPA4 knockdown required the participation of a series of apoptosis-related proteins. The downregulation of HSPA4 promoted the progression of CRC cells, which resulted in alterations of PI3K/Akt, CCND1 and CDK6 in downstream signaling pathways. Conclusions In sum, the downregulation of HSPA4 promoted CRC and may be a potential target for molecular therapy.

scholarly journals PIMREG, a Marker of Proliferation, Facilitates Aggressive Development of Cholangiocarcinoma Cells Partly Through Regulating Cell Cycle-Related Markers

2020 ◽  
Vol 19 ◽  
pp. 153303382097968
Author(s):  
Zhao-Ming Jiang ◽  
Hong-Bin Li ◽  
Shu-Guo Chen
Keyword(s):  
Cell Cycle ◽  
Western Blot ◽  
Cell Lines ◽  
Gene Set Enrichment Analysis ◽  
Cell Counting ◽  
Aberrant Expression ◽  
Gene Set ◽  
Invasion And Migration ◽  
The Public ◽  
And Migration

Background: Phosphatidylinositol binding clathrin assembly protein interacting mitotic regulator (PIMREG) is a protein associated with cell proliferation. Its aberrant expression was reported to be correlated with the development in multiple tumors. However, its role in cholangiocarcinoma (CAA) has not yet been evaluated in detail. Methods: Data were acquired from the public TCGA database for evaluating the expression pattern of PIMREG and assessing its clinical relevance as well as its correlation with overall survival. RBE and HUH28 cell lines were selected to perform loss- and gain-of-function of PIMREG assays respectively. Quantitative real-time PCR (RT-qPCR) and western blot analyses were used to measure the mRNA and protein levels of PIMREG. Cell Counting Kit-8, colony formation tests, and Transwell assays served to measure the effect of PIMREG on the proliferative, invasive and migratory capacities of CAA cells, appropriately. Gene set enrichment analysis (GSEA) was conducted to identify PIMREG associated gene set, which was further confirmed by western blot. Results: PIMREG was found to be highly expressed in CAA tissues and cell lines according to the public dataset and RT-qPCR analysis, and negatively related to the prognosis of patients with CAA. Moreover, knockdown of PIMREG suppressed and overexpression of PIMREG promoted the proliferation, invasion and migration of CAA cells. Furthermore, GSEA revealed that high PIMREG expression was positively associated with cell cycle signaling. And the next western blot analysis demonstrated that silencing PIMREG resulted in a reduction on the levels of p-CDK1, CCNE1, and CCNB1, whereas PIMREG overexpression led to an opposite result. Conclusion: The results suggested that PIMREG facilitates the growth, invasion and migration of CAA cells partly by regulating the cell cycle relative biomarkers, revealing that PIMREG may be a crucial molecule in the progression of CAA.

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 Tumor-Associated Macrophages (TAMs) in Colorectal Cancer (CRC): From Mechanism to Therapy and Prognosis

2021 ◽  
Vol 22 (16) ◽  
pp. 8470
Author(s):  
Hui Wang ◽  
Tian Tian ◽  
Jinhua Zhang
Keyword(s):  
Colorectal Cancer ◽  
Clinical Care ◽  
Inflammatory Cells ◽  
Genetic Alterations ◽  
Tumor Associated Macrophages ◽  
Invasion And Migration ◽  
Complex Process ◽  
Incidence And Mortality ◽  
And Migration

Colorectal cancer (CRC) is a malignant tumor in the digestive system whose incidence and mortality is high-ranking among tumors worldwide. The initiation and progression of CRC is a complex process involving genetic alterations in cancer cells and multiple factors from the surrounding tumor cell microenvironment. As accumulating evidence has shown, tumor-associated macrophages (TAMs)—as abundant and active infiltrated inflammatory cells in the tumor microenvironment (TME)—play a crucial role in CRC. This review focuses on the different mechanisms of TAM in CRC, including switching of phenotypical subtypes; promoting tumor proliferation, invasion, and migration; facilitating angiogenesis; mediating immunosuppression; regulating metabolism; and interacting with the microbiota. Although controversy remains in clinical evidence regarding the role of TAMs in CRC, clarifying their significance in therapy and the prognosis of CRC may shed new light on the optimization of TAM-centered approaches in clinical care.

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