scholarly journals Baicalein modulates the radiosensitivity of cervical cancer cells in vitro via miR-183 and the JAK2/STAT3 signaling pathway

2021 ◽  
Vol 30 (7) ◽  
pp. 0-0
Author(s):  
Hongwei Lei ◽  
Jingbin Shi ◽  
Yun Teng ◽  
Chenghui Song ◽  
Lijuan Zou ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Cervical Cancer Cells

scholarly journals Pancreatic cancer-educated macrophages protect cancer cells from complement-dependent cytotoxicity by up-regulation of CD59

2019 ◽  
Vol 10 (11) ◽  
Author(s):  
Ronghua Zhang ◽  
Qiaofei Liu ◽  
Junya Peng ◽  
Mengyi Wang ◽  
Xiang Gao ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Signaling Pathway ◽  
In Vitro Study ◽  
Stat3 Signaling ◽  
Pancreatic Cancer Cells ◽  
Complement Dependent Cytotoxicity ◽  
Stat3 Signaling Pathway

Abstract Tumor-associated macrophages (TAMs) are versatile immune cells that promote a variety of malignant behaviors of pancreatic cancer. CD59 is a GPI-anchored membrane protein that prevents complement activation by inhibiting the formation of the membrane attack complex, which may protect cancer cells from complement-dependent cytotoxicity (CDC). The interactions between CD59, TAMs and pancreatic cancer remain largely unknown. A tissue microarray of pancreatic cancer patients was used to evaluate the interrelationship of CD59 and TAMs and their survival impacts were analyzed. In a coculture system, THP-1 cells were used as a model to study the function of TAMs and the roles of pancreatic cancer-educated macrophages in regulating the expression of CD59 in pancreatic cancer cells were demonstrated by real-time PCR, western blot and immunofluorescence staining. The effects of macrophages on regulating CDC in pancreatic cancer cells were demonstrated by an in vitro study. To explore the potential mechanisms, RNA sequencing of pancreatic cancer cells with or without co-culture of THP-1 macrophages was performed, and the results showed that the IL-6R/STAT3 signaling pathway might participate in the regulation, which was further demonstrated by target-siRNA transfection, antibody neutralization and STAT3 inhibitors. Our data revealed that the infiltration of TAMs and the expression of CD59 of pancreatic cancer were paralleled, and higher infiltration of TAMs and higher expression of CD59 predicted worse survival of pancreatic cancer patients. Pancreatic cancer-educated macrophages could protect cancer cells from CDC by up-regulating CD59 via the IL-6R/STAT3 signaling pathway. These findings uncovered the novel mechanisms between TAMs and CD59, and contribute to providing a new promising target for the immunotherapy of pancreatic cancer.

scholarly journals Prosapogenin A induces apoptosis in human cancer cells in vitro via inhibition of the STAT3 signaling pathway and glycolysis

2013 ◽  
Vol 6 (5) ◽  
pp. 1323-1328 ◽  
Author(s):  
TIAN-XIAO WANG ◽  
ZHONG-QING ZHANG ◽  
YUE CONG ◽  
XIAO-YAN SHI ◽  
YING-HUA LIU ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Signaling Pathway ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

scholarly journals Ginsenoside Rg3 Inhibit The Proliferation And Metastasis of Cervical Cancer Cells in Vitro By Regulating NF-κB Signaling Pathway

2021 ◽  
Vol 5 (2) ◽  
Keyword(s):  
Cervical Cancer ◽  
Survival Rate ◽  
Protein Expression ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Hela Cells ◽  
Ginsenoside Rg3 ◽  
Cervical Cancer Cells ◽  
Proliferation And Metastasis

Objective: To investigate the effect and mechanism of ginsenoside Rg3 on the proliferation and metastasis of cervical. Methods: Cervical cancer cells HeLa were treated with different concentrations (0, 0.12, 0.24, 0.48 mmol/L) of ginsenoside Rg3, and then the survival rate of HeLa cells was detected by CCK-8 method, and the migration and invasion of HeLa cells were assessed using Transwell test, and expression of E-cadherin, N-cadherin, vimentin, Toll receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), phosphorylated nuclear transcription factor κB p65 (P-NF-κB p65) proteins were calculated by Western blot. Results: After ginsenoside Rg3 (0.12, 0.24, 0.48 mmol/L) treatment, the survival rate, migration number, invasion number, and N-cadherer number, and N-cadherin, Vimentin, TLR4, MyD88, p-NF-κB p65 protein expression of HeLa cells were significantly reduced (P<0.05) Ginsenoside protein expression was significantly increased (P<0.05), and showed a concentration-dependent relationship. Conclusion: Ginsenoside Rg3 could inhibit the proliferation and metastasis of cervical cancer cells in vitro, and its mechanism might be related to the inhibition of NF-κB signaling pathway.

scholarly journals Plasma-based Endogenous Metabolomics Profiling of High-Risk Human Papillomavirus and Their Emerging Roles in the Progression of Cervical Cancer

2021 ◽  
Author(s):  
Qin Wang ◽  
Min Xu ◽  
Tingting Chen ◽  
Jing Chen ◽  
Runjie Zhang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
High Risk ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Metabolic Phenotype ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

Abstract Objective: High-risk human papillomavirus (HR-HPV) is the main etiological factor for cervical cancer. Accumulating evidence has suggested that the active role of metabolites in the initiation and progression of cancers. This study was to explore the metabolic profiles of HR-HPV infection and their potential functions in cervical cancer.Methods: Non-targeted metabolomics approach was used to detect metabolic alterations in the plasma obtained from HPV-16 positive (HPV16 (+)), HPV-18 positive (HPV18 (+)) and HPV negative (CTL) individuals, followed by CCK8 experiment to detect the effect of different metabolites on the proliferation of Hela and GH354. A cell migration test then verified significant metabolites on the migration of Hela and GH354. Q RT-qPCR and western blot were used to detect malignant progression related mRNA and protein expression levels of cervical cancer.Results: HR-HPV groups shared 24 dysregulated metabolites (such as amino acids, ceramides, glycerophosphocholines). Further experiments showed ceramide species, including C8 inhibits cervical cancer cells proliferation and migration in vitro. In contrast, C12 significantly enhanced cervical cancer cells proliferation and migration in vitro. Protein and mRNA expressions indicated C8 and C12 were related to the malignant behavior of cervical cancer in vitro. The underlying mechanism demonstrated that C8 intervention inhibited proliferation and migration in cervical cancer cells via the MAPK/JNK signaling pathway, while C12 intervention promoted proliferation and migration in cervical cancer cells via the MAPK/ERK signaling pathway. These findings may contribute to the treatment of HR-HPV-induced cervical cancer by intervening in its initiation and progression.Conclusion: Our study shed some light on how metabolites influenced the relationship between HR-HPV oncogenic capability and metabolic phenotype change and identify species C8 and C12 as critical lipid metabolites that modulate cervical cancer cell’s function.

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