scholarly journals Hydrogen gas represses the progression of lung cancer via down-regulating CD47

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Jinghong Meng ◽  
Leyuan Liu ◽  
Dongchang Wang ◽  
Zhenfeng Yan ◽  
Gang Chen
Keyword(s):  
Lung Cancer ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Hydrogen Gas ◽  
Cell Counting ◽  
Dependent Manner ◽  
Expression Levels ◽  
Invasion And Migration ◽  
Tumor Tissues ◽  
And Migration

Abstract Hydrogen gas (H2) has been identified to play an anti-tumor role in several kinds of cancers, but the molecular mechanisms remain largely unknown. In our previous study, our project group found that H2 could decrease the expression of CD47 in lung cancer A549 cells via the next-generation sequencing, indicating that CD47 might be involved in H2-mediated lung cancer repression. Therefore, the present study aimed to explore the effects of CD47 on H2-induced lung cancer repression. Western blotting and real-time PCR (RT-PCR) assays were used to detect the levels of proteins and mRNAs, respectively. Cell proliferation, invasion, migration and apoptosis were detected by using the cell counting kit-8 (CCK-8), Transwell chambers, wound healing and flow cytometry assays, respectively. The results showed that H2 treatment caused decreases in the expression levels of CD47 and cell division control protein 42 (CDC42) in a dose-dependent manner. Up-regulation of CD47 abolished H2 roles in promoting lung cancer cell apoptosis and repressing cell growth, invasion and migration in both A549 and H1975 cell lines. However, knockdown of CD47 enhanced H2 role in lung cancer inhibition. Moreover, we also observed that H2 treatment induced obvious inhibitions in the expression levels of CDC42 and CD47 in mice tumor tissues, as well as reinforced macrophage-mediated phagocytosis in A549 and H1975 cells. In conclusion, the current study reveals that H2 inhibits the progression of lung cancer via down-regulating CD47, which might be a potent method for lung cancer treatment.

scholarly journals LINC00476 suppresses the progression of non-small cell lung cancer via inducing the ubiquitination of SETDB1

2020 ◽  
Author(s):  
Guanghui Cui ◽  
Xiao Fu ◽  
Wentao Wang ◽  
Xiaofang Chen ◽  
Shuaishuai Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Cell Counting ◽  
Small Cell Lung ◽  
Invasion And Migration ◽  
Tumor Tissues ◽  
And Migration

Abstract Background: Long non-coding RNAs are involved in the tumorigenesis of non-small cell lung cancer (NSCLC). This study aims to investigate whether LINC00476 affects the proliferation, invasion, and migration of NSCLC cells via SETDB1-activated Wnt/β-catenin pathway. Method: The expression of LINC00476, SETDB1, Wnt1, and β-catenin were determined in NSCLC tumor tissues and the paired adjacent tissues, as well as in NSCLC cell lines and bronchial epithelioid cell lines. Cell proliferation, invasion, and migration were determined using cell counting kit-8 assay and Transwell assay. The relationship between LINC00476 and SETDB1 was elucidated using RNA pull-down, RNA immunoprecipitation, and ubiquitination assays. Result: LINC00476 was significantly downregulated, while SETDB1, Wnt1, and β-catenin were upregulated in NSCLC tumor tissues and cell lines compared to the normal ones. Overexpression of LINC00476 promoted the proliferation, invasion, and migration of NSCLC cells, as well as suppressed tumor growth in the mouse xenograft. Meanwhile, overexpression of LINC00476 induced the degradation of SETDB1 via promoting its ubiquitination. The simultaneous overexpression of LINC00476 and SETDB1 negated the inhibition of LINC00476 overexpression on the proliferation, invasion, and migration of NSCLC cells. Conclusion: LINC00476 acts as a tumor suppressor in NSCLC via downregulating SETDB1, which provides a novel target in treating NSCLC.

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.

Knockdown CYP2S1 inhibits lung cancer cells proliferation and migration

2021 ◽  
pp. 1-9
Author(s):  
Huan Guo ◽  
Baozhen Zeng ◽  
Liqiong Wang ◽  
Chunlei Ge ◽  
Xianglin Zuo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Lung Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

BACKGROUND: The incidence of lung cancer in Yunnan area ranks firstly in the world and underlying molecular mechanisms of lung cancer in Yunnan region are still unclear. We screened a novel potential oncogene CYP2S1 used mRNA microassay and bioinformation database. The function of CYP2S1 in lung cancer has not been reported. OBJECTIVE: To investigate the functions of CYP2S1 in lung cancer. METHODS: Immunohistochemistry and Real-time PCR were used to verify the expression of CYP2S1. Colony formation and Transwell assays were used to determine cell proliferation, invasion and migration. Xenograft assays were used to detected cell growth in vivo. RESULTS: CYP2S1 is significantly up-regulated in lung cancer tissues and cells. Knockdown CYP2S1 in lung cancer cells resulted in decrease cell proliferation, invasion and migration in vitro. Animal experiments showed downregulation of CYP2S1 inhibited lung cancer cell growth in vivo. GSEA analysis suggested that CYP2S1 played functions by regulating E2F targets and G2M checkpoint pathway which involved in cell cycle. Kaplan-Meier analysis indicated that patients with high CYP2S1 had markedly shorter event overall survival (OS) time. CONCLUSIONS: Our data demonstrate that CYP2S1 exerts tumor suppressor function in lung cancer. The high expression of CYP2S1 is an unfavorable prognostic marker for patient survival.

scholarly journals miR-103 Functions as a Tumor Suppressor by Directly Targeting Programmed Cell Death 10 in NSCLC

2018 ◽  
Vol 26 (4) ◽  
pp. 519-528 ◽  
Author(s):  
Dong Yang ◽  
Jian-Jun Wang ◽  
Jin-Song Li ◽  
Qian-Yu Xu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Tumor Size ◽  
Apoptotic Cell ◽  
A549 Cells ◽  
Invasion And Migration ◽  
Metastatic Capacity ◽  
And Migration

Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancer cases. Absence of miR-103 has recently been identified to be associated with metastatic capacity of primary lung tumors. However, the exact role of miR-103 in NSCLC and the molecular mechanism are unclear. In the present study, we showed that miR-103 expression was reduced in NSCLC tissues and cells. miR-103 expression was negatively correlated with tumor size and stage. The overall survival was longer in patients with higher miR-103 level than in those with lower miR-103 expression. miR-103 inhibited cell proliferation in A549 cells, decreased tumor weight and volume, and prolonged survival of tumor-implanted nude mice. miR-103 increased apoptotic cell death in A549 cells. Furthermore, miR-103 decreased the invasion and migration abilities in A549 cells, as evidenced by Transwell and wound healing results. Downregulation of miR-103 significantly reduced the level of programmed cell death 10 (PDCD10). We found a significant decrease in the relative luciferase activity of the reporter gene in A549 cells cotransfected with the miR-103 mimic and pGL3-PDCD10 WT 3′-UTR, but not pGL3-PDCD10 mut 3′-UTR. We showed that overexpression of PDCD10 significantly inhibited miR-103-induced inhibition of cell proliferation, increased apoptosis, and decreased invasion and migration in A549 cells. Moreover, we found that PDCD10 expression was increased in NSCLC tissues and cells. PDCD10 expression was positively correlated with tumor size and stage. Overexpression of PDCD10 increased cell proliferation and inhibited apoptosis in A549 cells. The data demonstrated that dysregulation of the miR-103/PDCD10 signal may be a novel therapeutic target for the treatment of NSCLC.

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.

Inhibition of PLOD3 Suppresses Proliferation, Invasion and Migration of Breast Cancer Cells

2019 ◽  
Vol 9 (11) ◽  
pp. 1528-1534
Author(s):  
Shiqiong Su ◽  
Qing Ni ◽  
Jing Hou
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Western Blotting ◽  
Molecular Mechanisms ◽  
Treatment Strategies ◽  
Cell Counting ◽  
Matrix Metalloproteinase 2 ◽  
Invasion And Migration ◽  
And Migration ◽  
Interfering Rna

Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 3 (PLOD3) has been reported to be involved in various human cancers. However, the function of PLOD3 in breast cancer (BC) has not been addressed. This research attempted to probe the effects and molecular mechanisms of PLOD3 in BC. The expression of PLOD3 was examined by Western blotting and RT-qPCR in several BC cell lines and nontumorigenic breast MCF-10A cells. Then, PLOD3 was silenced by transfecting with small interfering RNA (siRNA). Cell proliferation was measured by Cell Counting Kit-8 assay and cell cycle was evaluated by flow cytometry assay after transfection. Subsequently, wound healing assay and Transwell assay were exploited for detecting the abilities of cell invasion and migration, respectively. In addition, the expression of proliferation- and migration-related genes were examined by Western blotting. The results revealed that the expression of PLOD3 was upregulated in BC cell lines compared with MCF-10A cells. PLOD3 silencing suppressed the proliferative ability of BC cells, enhanced the ratio of cells in the G1 and G2 phases and reduced those in the S phase. Moreover, the expression of Ki67 and cyclinD1 were significantly downregulated, accompanied by an upregulation in p27 expression after transfection with PLOD3 siRNA. Furthermore, inhibition of PLOD3 restrained invasion and migration of BC cells coupled with a reduced expression of matrix metalloproteinase 2 (MMP2) and MMP9. The explorations unveiled that PLOD3 silencing restrained proliferation, invasion and migration of BC cells, which provides theoretical basis and treatment strategies for the treatment of BC.

scholarly journals MiR-454-3p and miR-374b-5p suppress migration and invasion of bladder cancer cells through targetting ZEB2

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Suogang Wang ◽  
Geng Zhang ◽  
Wanxiang Zheng ◽  
Qin Xue ◽  
Di Wei ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Migration And Invasion ◽  
Pcr Analysis ◽  
Inhibitory Effects ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Invasion And Migration ◽  
And Migration

Bladder cancer (BCa) threatens human health due to the high occurrence and mortality. Nowadays, more and more researchers focussed on the molecular mechanisms and biological functions of miRNAs in human cancers. The present study aims to study the biological role of miR-454-3p and miR-374b-5p in BCa. The expression levels of miR-454-3p and miR-374b-5p were detected in BCa tissues and cell lines by qRT-PCR analysis. Kaplan–Meier analysis revealed that the expression levels of miR-454-3p and miR-374b-5p were positively correlated with the overall survival (OS) rate of BCa patients. Gain-of-function assays were conducted to demonstrate the inhibitory effects of miR-454-3p and miR-374b-5p on the invasion, migration, and epithelial–mesenchymal transition (EMT) of BCa cells. Mechanically, ZEB2 was found to be a target of both miR-454-3p and miR-374b-5p. Rescue assays revealed that ZEB2 reversed the inhibitory effects of miR-454-3p and miR-374b-5p on the invasion and migration of BCa cell lines. In summary, miR-454-3p and miR-374b-5p negatively regulated invasion and migration of BCa cell lines via targetting ZEB2.

scholarly journals SDC1 knockdown induces epithelial–mesenchymal transition and invasion of gallbladder cancer cells via the ERK/Snail pathway

2020 ◽  
Vol 48 (8) ◽  
pp. 030006052094788
Author(s):  
Zixiang Liu ◽  
Hao Jin ◽  
Song Yang ◽  
Haiming Cao ◽  
Ziyan Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Gallbladder Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Negative Control ◽  
Cell Counting ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Invasion And Migration ◽  
And Migration ◽  
E Cadherin

Background Expression levels of the cell adhesion molecule syndecan-1 (SDC1) have been shown to be inversely proportional to tumor differentiation and prognosis. However, its role in the development of gallbladder cancer (GBC) remains unclear. Methods We knocked down SDC1 in GBC cells by RNA interference and determined its roles in cell proliferation, apoptosis, invasion, and migration by Cell Counting Kit-8, colony-formation, flow cytometry, Hoechst 33342 staining, transwell invasion, and scratch wound assays. Expression levels of epithelial–mesenchymal transition (EMT)-related and extracellular signal-regulated kinase (ERK)/Snail pathway proteins were determined by western blotting and immunofluorescence. Results Cell proliferation, invasion, and migration were all increased in GBC cells with SDC1 knockdown, compared with cells in the blank control and negative control groups, but apoptosis was similar in all three groups. E-cadherin and β-catenin expression levels were significantly lower and N-cadherin, vimentin, p-ERK1/2, and Snail expression were significantly higher in the SDC1 knockdown group compared with both controls, while ERK1/2 levels were similar in all groups. Reduced E-cadherin and increased vimentin levels were confirmed by immunofluorescence. Conclusions SDC1 knockdown promotes the proliferation, invasion, and migration of GBC cells, possibly by regulating ERK/Snail signaling and inducing EMT and cancer cell invasion.

scholarly journals TRAF7 contributes to tumor progression by promoting ubiquitin-proteasome mediated degradation of P53 in hepatocellular carcinoma

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Qi Zhang ◽  
Xinqi Zhang ◽  
Weiguo Dong
Keyword(s):  
Hepatocellular Carcinoma ◽  
Molecular Mechanisms ◽  
Tumor Development ◽  
Invasion And Migration ◽  
Tumor Tissues ◽  
Prevention And Treatment ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway ◽  
And Migration ◽  
Hcc Cells

AbstractIt has been proved that TRAFs family proteins played malfunctioning roles in the development of human cancers. TRAF7 is the last one of TRAFs family proteins to be found, which was demonstrated to be involved in a serious of cancers development. In this study, we systematically investigated the molecular mechanisms of TRAF7 in facilitating hepatocellular carcinoma (HCC). We discovered that TRAF7 was overexpressed in tumor tissues and the increased TRAF7 expression was closely associated with tumor size, histologic grade, TNM stage and poor prognostication. TRAF7 overexpression repressed cell apoptosis and promoted cell proliferation, invasion and migration, whereas knockdown of TRAF7 in HCC cells had totally opposite effects. Besides, we identified the interaction between TRAF7 and P53 in HCC and demonstrated that TRAF7 promoted ubiquitin-proteasome mediated degradation of P53 at K48 site. The rescue assays further proved that the function of TRAF7 in inhibiting apoptosis and promoting tumor development was depended on P53 in HCC. Overall, this work identified that TARF7 promoted tumorigenesis by targeted degradation P53 for ubiquitin-mediated proteasome pathway. Targeting the TRAF7-P53 axis may provide new insights in the pathogenesis of HCC, and pave the way for developing novel strategies for HCC prevention and treatment.

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