scholarly journals Allicin depresses biological activities of pancreatic cancer cells by regulating miRNA-339-5p/ZNF-689 axis

2021 ◽  
Author(s):  
Zeqian Yu ◽  
Susu Zhao
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Biological Activities ◽  
Caspase 8 ◽  
Vimentin Expression ◽  
Invasion And Migration ◽  
And Migration ◽  
E Cadherin

IntroductionThe aim of this study was to discuss Allicin’s anti-tumor effects and relative in pancreatic cancer cell via vitro and vivo study.Material and methodsUsing PANC-1 and Hs766T cell as research cell lines in our study. The PANC-1 abd GS799T cell were respectively treated with difference concentrations of Allicin. In next step, the PANC-1 abd GS799T cell were transfected with si-miRNA-339-5p which knockdown miRNA-339-5p. The cells were treated with difference concentration of Allicin. Measuring cell proliferation, apoptosis, invasion and migration by MTT, EDU, flow cytometry, TUNEL, transwell and wound healing assay. Relative gene (miRNA-339-5p, ZNF-689, Caspase-3, Caspase-8, E-cadherin and Vimentin) and protein (ZNF-689, Caspase-3, Caspase-8, E-cadherin and Vimentin) expression were evaluated by RT-qPCR and WB assay.ResultsAllicin had effects to suppress PANC-1 and Hs766T cell biological activities including cell proliferation, invasion and migration with cell apoptosis significantly increasing, however, with si-miRNA-339-5p which inhibit miRNA-339-5p expression transfection, the cells biological activities enhancing with cell apoptosis depressing, Compared with NC group, miRNA-339-5p, Caspase-3, Caspase-8 and E-cadherin expression were significantly increased and ZNF-689 and Vimentin expression were significantly depressed in Allicin treated groups, however, with miRNA-339-5p inhibitor transfection, the Allicin’s effects significantly disappear.ConclusionsAllicin had anti-tumor effect to pancreatic cancer biological activities via regulation miRNA-339-5p/ZNF-689 axis in vitro study.

lncRNA UBE2R2-AS1 Had Anti-Tumor Effects in Non-Small Cell Lung Cancer

2019 ◽  
Vol 9 (12) ◽  
pp. 1685-1692
Author(s):  
Haiyun Zhang ◽  
Weidong Han ◽  
Haimei Liu ◽  
Haijun Chen
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Cell Number ◽  
Caspase 8 ◽  
Down Regulation ◽  
Invasion And Migration ◽  
Protein Levels ◽  
And Migration

Background: The purpose of our work was to discuss anti-tumor effects and mechanisms of lncRNA UBE2R2-AS1 in NSCLC. Methods : lncRNA UBE2R2-AS1 gene level was measured by RT-qPCR in BEAS-2B, A549, H1975, H1650 and HCC827. Dividing A549 and H1650 cells into NC, Vector and UBE2R2-AS1. Measuring the cell proliferation by CCK-8 assay; Using flow cytometer to evaluate cell apoptosis, using transwell and wound healing methods to evaluate invasion and migration abilities. The relative protein expressions were measured by WB assay. Results: UBE2R2-AS1 mRNA expression of A549 and H1650 were the lowest in all cells lines. With UBE2R2-AS1 transfection, the cell proliferation rates were significantly down-regulation with cell apoptosis significantly increasing (P < 0 001). Meanwhile, the invasion cell number and wound healing rates of UBE2R2-AS1 groups were significantly depressed (P < 0 001). Bcl-2, TLR4 and MyD88 proteins expressions were significantly down-regulation and Caspase-3 and Caspase-8 proteins levels were significantly upregulation in UBE2R2-AS1 groups (P < 0 001). Conclusion: UBE2R2-AS1 overexpression had antitumor in NSCLC, the mechanisms might be correlation with regulation Bcl-2, caspase-3, caspase-8, TLR4 and MyD88 protein levels.

scholarly journals Amygdalin promotes the activity of T cells to suppress the progression of HBV-related hepatocellular carcinoma via the JAK2/STAT3 signaling pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ruoyu Wang ◽  
Dong Zhang ◽  
Kewei Sun ◽  
Jianping Peng ◽  
Wenfang Zhu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Cell Viability ◽  
Caspase 3 ◽  
Invasion And Migration ◽  
Ifn Γ ◽  
And Migration ◽  
Cellular Immune

Abstract Background Hepatitis B virus (HBV) infection is a high-risk factor of hepatocellular carcinoma (HCC). Cellular immune responses are essential for HCC development, and the CD4+ and CD8+ T subtypes are identified as the primary anti-tumor immune cells. In the study, we investigated the effect and mechanism of amygdalin in the cellular immune response in HBV-related HCC and HCC progression. Methods The cell proliferation was examined by MTT analysis. Cells metastasis ability was detected by Invasion and migration assays. Quantification of apoptotic cells was performed with Flow cytometer assay. The protein levels of p-STAT3, STAT3, p-JAK2, JAK2, caspase-3, cleaved caspase-3 were detected by performing immunoblotting assays. Results We demonstrate that amygdalin treatment could rescue the HBV-T cell viability and IFN-γ and TNF-αproduction. In HBV-T cells, the MFI levels of CD8+ are lower than that in NC-T cells. Moreover, the phosphorylation levels of STAT3 and JAK2 are higher in HBV-T cells, compared to those in NC-T cells, and then reduced by amygdalin treatment. Co-culture with HBV-T cells could reduce IFN-γ and TNF-α, production while increase IL-6 and IL-10 production in HepG2.2.15 cells; these alterations could be partially reversed by amygdalin pretreatment. Finally, co-culture with HBV-T cells significantly promoted the cell viability, inhibited the apoptosis, and promoted the migration of HepG2.2.15 cells, and these alterations could be partially reversed by amygdalin treatment. Conclusion Our findings provide a rationale for further studies on the functions and mechanism of amygdalin inhibiting HBV-related HCC cell proliferation, invasion, and migration via T cell-mediated tumor immunity.

scholarly journals FGFR3 promotes the growth and malignancy of melanoma by influencing EMT and the phosphorylation of ERK, AKT, and EGFR

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Lei Li ◽  
Shuai Zhang ◽  
Hao Li ◽  
Haiyan Chou
Keyword(s):  
Cell Proliferation ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Colony Formation ◽  
Caspase 3 ◽  
Growth Factor Receptor ◽  
Invasion And Migration ◽  
Node Metastasis ◽  
And Migration

Abstract Background Overexpression of fibroblast growth factor receptor 3 (FGFR3) has been linked to tumor progression in many types of cancer. The role of FGFR3 in melanoma remains unclear. In this study, we aimed to uncover the role of FGFR3 in the growth and metastasis of melanoma. Methods FGFR3 knockdown and overexpression strategies were employed to investigate the effects of FGFR3 on colony formation, cell apoptosis, proliferation, migration, and in vitro invasion, along with the growth and metastasis of melanoma in a xenografts mouse model. The protein expression levels of extracellular signal-regulated kinase (ERK), protein kinase B (AKT), epidermal growth factor receptor (EGFR), and epithelial-mesenchymal transition (EMT) markers were determined by Western blot analysis. Results The mRNA expression of FGFR3 was higher in melanoma tissues than normal healthy tissues. FGFR3 expression in cutaneous malignant melanoma (CMM) tissues was positively correlated with the Breslow thickness and lymph node metastasis. In A357 cells, knockdown of the FGFR3 gene decreased the colony formation ability, cell proliferation, invasion, and migration, but increased the caspase 3 activity and the apoptosis rate; overexpression of FGFR3 increased the colony formation ability, cell proliferation, invasion, and migration, but decreased the caspase 3 activity and apoptosis rates. FGFR3 knockdown also upregulated E-cadherin, downregulated N-cadherin and vimentin, and decreased the phosphorylation levels of ERK, AKT, and EGFR. In the MCC xenografts mice, knockdown of FGFR3 decreased tumor growth and metastasis. Conclusions FGFR3, which is highly expressed in CMM tissues, is correlated with increased Breslow thickness and lymph node metastasis. FGFR3 promotes melanoma growth, metastasis, and EMT behaviors, likely by affecting the phosphorylation levels of ERK, AKT, and EGFR.

Circ_0085296 suppresses trophoblast cell proliferation, invasion, and migration via modulating miR-144/E-cadherin axis

Placenta ◽  
2020 ◽  
Vol 97 ◽  
pp. 18-25
Author(s):  
Hailing Zhu ◽  
Xia Niu ◽  
Qinghua Li ◽  
Yuehua Zhao ◽  
Xue Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Trophoblast Cell ◽  
Invasion And Migration ◽  
And Migration ◽  
E Cadherin

LncRNA CEACAMP8 Regulates the Proliferation, Invasion and Migration of Trophoblast Cells

2019 ◽  
Vol 9 (9) ◽  
pp. 1215-1221
Author(s):  
Li Jie ◽  
Zhangcai Zheng ◽  
Liping Liu ◽  
Yali Liu ◽  
Zhaoyan Meng ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Flow Cytometry Analysis ◽  
Trophoblast Cells ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Qpcr Analysis ◽  
And Migration ◽  
E Cadherin

Preeclampsia (PE) is an idiopathic hypertension syndrome occurring after 20 weeks of gestation. Reports showed that lncRNAs expression was abnormal in preeclampsia. We aimed to investigate the role of lncRNA CEACAMP8 in the proliferation, invasion and migration of trophoblast cells to improve the preeclampsia. The cell transfection effects were determined by RT-qPCR analysis. The proliferation, invasion and migration of HTR-8/SVneo cells were detected by CCK-8 assay, transwell assay and wound healing assay. The flow cytometry analysis analyzed the cell cycle. Moreover, the expression of CDK2, cyclinD1, P21, MMP2, MMP9, E-cadherin, b-catenin and vimentin was determined by the western blot analysis. Consequently, CEACAMP8 inhibition promoted the proliferation, invasion and migration of HTR-8/SVneo cells and kept most of the cells in the S phase. The expression of proteins related to the proliferation, invasion and migration of HTR-8/SVneo cells were also changed in accordance with the increase of proliferation, invasion and migration of HTR-8/SVneo cells. In addition, lncRNA CEACAMP8 inhibition decreased the expression of E-cadherin and b-catenin, and increased the vimentin expression to promote the epithelial-mesenchymal transition. And, CEACAMP8 overexpression could reverse the above changes. This study indicated that CEACAMP8 inhibition promoted the proliferation, invasion and migration of HTR-8/SVneo cells and lncRNA CEACAMP8 overexpression reversed.

scholarly journals Chlorophenyl-benzoxime inhibits pancreatic cancer cell proliferation, invasion and migration by down-regulating the expressions of interleukin-8 and cyclooxygenase-2

2021 ◽  
Vol 18 (7) ◽  
pp. 1413-1418
Author(s):  
Pinyan Wang ◽  
Yanan Xue ◽  
Xiao Yu
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Western Blotting ◽  
Mtt Assay ◽  
Quantitative Polymerase Chain Reaction ◽  
Cyclooxygenase 2 ◽  
Interleukin 8 ◽  
Invasion And Migration ◽  
Cox 2 ◽  
And Migration

Purpose: To investigate the effects of chlorophenyl-benzoxime (CPBZX) on pancreatic cancer (PC) cell proliferation, invasion and migration, and the underlying mechanism of action. Methods: Pancreatic carcinoma cell lines (HuP-T4, HuP-T3 and BxPC-3) were cultured in Dulbecco's Modified Eagle medium (DMEM) containing 10 % fetal bovine serum (FBS), penicillin (100 U/mL) and streptomycin (10 μg/mL) at 37 ˚C in a humidified atmosphere containing 5 % CO2 and 95 % air. Cell proliferation was assessed using MTT assay. Real-time quantitative polymerase chain reaction (qRTPCR) and Western blotting were employed for the determination of changes in the levels of expression of carcinoembryonic antigen (CEA), interleukin-8 (IL-8) and cyclooxygenase-2 (COX 2). Cell invasion and migration were determined using Transwell and wound healing assays, respectively. Results: The results of MTT assay showed that CPBZX significantly and dose-dependently inhibited the proliferation of PC cells (p < 0.05). Incubation of HuP-T4 cells with CPBZX significantly and dosedependently reduced the invasive ability of the cells (p < 0.05). The migratory ability of HuP-T4 cells was also significantly and dose-dependently inhibited by CPBZX (p < 0.05). The results of Western blotting and qRT PCR showed that CPBZX treatment significantly and dose-dependently upregulated CEA mRNA expression (p < 0.05). On the other hand, the expressions of IL-8 and COX-2 were significantly and dose-dependently down-regulated by CPBZX. Treatment of pancreatic tumor mice with CPBZX significantly decreased tumor growth and metastasis of tumor cells to the pulmonary tissues, liver and lymph nodes (p < 0.05). Conclusion: The results of this study suggest that CPBZX inhibits the development and metastasis of PC via the down-regulation of IL-8 and COX 2 expressions, and therefore may find application in pancreatic cancer therapy.

scholarly journals Carnosol Induces Cell Apoptosis and Inhibits Invasion and Proliferation in Skin Epidermoid Cancer in Vitro Through MMP11-EGFR Pathway

2021 ◽  
Author(s):  
Shiqiu Jiang ◽  
Hairong Liu ◽  
Jie Zhang ◽  
Fang Zhang ◽  
Jiawei Fan
Keyword(s):  
Cell Proliferation ◽  
Overall Survival ◽  
Skin Cancer ◽  
Mrna Expression ◽  
Cell Apoptosis ◽  
Survival Rates ◽  
Invasion And Migration ◽  
Egfr Expression ◽  
E Cadherin

Abstract Background and purpose: The anti-tumor effect of carnosol has been revealed in cancers. This research intends to explore the role and underlying mechanisms of carnosol in the skin cancer in vitro. Methods: Online database GEPIA was used to preliminarily analyze MMP11 expression in skin cancer and further performed overall survival evaluation based on TCGA data. 0, 5µM, 10 µM, 20 µM carnosol was added into the skin cancer A431 cell culture. Later, RT-PCR method detected the mRNA expression of MMP-11 and Elisa kits measured the concentrations of MMP11, phosphor-EGFR and total EGFR proteins as well as the biomarkers related to proliferation (Ki67) and EMT (E-cadherin and Vimentin) as well as Casepase-3. The 20µM carnosol group was selected to further study the regulatory effect of MMP11 in A431 cells.Colony formation examined the cell proliferation. Flow cytometry method checked cell apoptosis while Transwell method explored the cell invasion and migration. Results: MMP11 is upregulated in skin cancer and lower level of MMP11 or EGFR expression is correlated with higher overall survival rates. Carnosol addition inhibited the mRNA expression of MMP11 and lowered the protein concentrations of MMP11 and phosphor-EGFR. In addition, Ki67 and Vimentin concentration was inhibited by carnosol while E-cadherin was instead promoted. Caspase-3 activity was enhanced by carnosol. Upregulation of MMP11 recovered EGFR activation, cell proliferation and invasion while inhibited apoptosis, partly counteracted the function of carnosol in cells. Conclusion: Carnosol might induce cell apoptosis and inhibits invasion and proliferation in skin epidermoid cancer in vitro through MMP11-EGFR pathway.

Silencing Circ_0005075 Inhibits the Invasion and Migration of Colon Cancer Cells and Induces Apoptosis

2021 ◽  
Vol 11 (3) ◽  
pp. 426-432
Author(s):  
Xiancheng Kong ◽  
Hao Zhang ◽  
Jianping Huang ◽  
Liang Yan ◽  
Li Sha ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Mirna Regulation ◽  
Migration Ability ◽  
Vimentin Expression ◽  
Sw620 Cell ◽  
Invasion And Migration ◽  
Sw620 Cells ◽  
And Migration ◽  
E Cadherin

Colon cancer is a common malignancy of the digestive tract, mostly occurring at the junction of the rectum and colon. It easily invades multiple internal organs and tissues, causing systemic injury and mortality to patients. The occurrence and development of colon cancer involve multiple genes and multiple factors. It is greatly significant to identify oncogenes and tumor suppressor genes that influence the development of colon cancer and to study their mechanism of action for colon cancer diagnosis and treatment. Furthermore, circRNA are involved in the development of several types of tumors by affecting miRNA regulation on target gene expression. In the present study, circ_0005075 siRNA and circ_0005075 siRNA + mir-335 inhibitor were transfected into colon cancer SW620 cells, and circ_0005075 gene expression was significantly decreased after transfecting circ_0005075 siRNA into SW620 cells. Silencing circ_0005075 expression significantly inhibited SW620 cell proliferation, invasion, and migration, and promoted apoptosis, downregulated PCNA and vimentin expression, and upregulated E-cadherin and cleaved caspase3 expression. After circ_0005075 siRNA + mir-335 was transfected, it inhibited circ_0005075 and mir-335 expression, which significantly affected the vigor, invasion and migration ability, apoptosis rate of SW620 cells, as well as PCNA, E-cadherin, vimentin, and cleaved caspase3 expression. Therefore, the present study demonstrated that circ_0005075 silencing inhibited the proliferation, invasion, and migration of SW620 cells and promoted apoptosis by upregulating mir-335 expression.

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