A comparative study on the mechanisms of anti-lung cancer activities of three sulfated galactofucans

2021 ◽  
Author(s):  
Wenjing Zhang ◽  
Wanli Wu ◽  
Yizhong Bao ◽  
Xiaojun Yan ◽  
Fu-Ming Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Comparative Study ◽  
Sargassum Thunbergii ◽  
Anti Tumor Activity

Abstract: Sulfated galactofucans, as the active compositions of fucoidan, were reported to exhibit anti-tumor activity. In the current study, a sulfated galactofucan (SGF) from Sargassum thunbergii and its three derivatives...

Enhancement of gold-nanocluster-mediated chemotherapeutic efficiency of cisplatin in lung cancer

2021 ◽  
Author(s):  
Mei Jiang ◽  
Yuchen Lin ◽  
Xiaocui Fang ◽  
Mingpeng Liu ◽  
Lilusi Ma ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Therapy ◽  
Delivery System ◽  
Gold Nanoclusters ◽  
Cationic Peptide ◽  
Gold Nanocluster ◽  
Lung Cancer Therapy ◽  
Anti Tumor Activity

A novel delivery system for cisplatin based on electrostatics-mediated assemblies of gold nanoclusters and PEGylated cationic peptide was constructed. The constructed cisplatin@GC-pKs showed much enhanced anti-tumor activity for lung cancer therapy.

scholarly journals Anti-tumor activity of tanshinone IIA in combined with cyclophosphamide against Lewis mice with lung cancer

2016 ◽  
Vol 9 (11) ◽  
pp. 1084-1088 ◽  
Author(s):  
Qi Li ◽  
Ke Hu ◽  
Si Tang ◽  
Li-Fang Xu ◽  
Yu-Chuan Luo
Keyword(s):  
Lung Cancer ◽  
Tanshinone Iia ◽  
Anti Tumor Activity

scholarly journals Prodigiosin-Emerged PI3K/Beclin-1-Independent Pathway Elicits Autophagic Cell Death in Doxorubicin-Sensitive and -Resistant Lung Cancer

2018 ◽  
Vol 7 (10) ◽  
pp. 321 ◽  
Author(s):  
Wei-Jun Chiu ◽  
Shian-Ren Lin ◽  
Yu-Hsin Chen ◽  
May-Jwan Tsai ◽  
Max Leong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Mammalian Target Of Rapamycin ◽  
Underlying Mechanism ◽  
Beclin 1 ◽  
Class Iii ◽  
Microtubule Associated Proteins ◽  
Associated Proteins ◽  
Anti Tumor Activity

Prodigiosin (PG) belongs to a family of prodiginines isolated from gram-negative bacteria. It is a water insoluble red pigment and a potent proapoptotic compound. This study elucidates the anti-tumor activity and underlying mechanism of PG in doxorubicin-sensitive (Dox-S) and doxorubicin-resistant (Dox-R) lung cancer cells. The cytotoxicity and cell death characteristics of PG in two cells were measured by MTT assay, cell cycle analysis, and apoptosis/autophagic marker analysis. Then, the potential mechanism of PG-induced cell death was evaluated through the phosphatidylinositol-4,5-bisphosphate 3-kinase-p85/Protein kinase B /mammalian target of rapamycin (PI3K-p85/Akt/mTOR) and Beclin-1/phosphatidylinositol-4,5-bisphosphate 3-kinase-Class III (Beclin-1/PI3K-Class III) signaling. Finally, in vivo efficacy was examined by intratracheal inoculation and treatment. There was similar cytotoxicity with PG in both Dox-S and Dox-R cells, where the half maximal inhibitory concentrations (IC50) were all in 10 μM. Based on a non-significant increase in the sub-G1 phase with an increase of microtubule-associated proteins 1A/1B light chain 3B-phosphatidylethanolamine conjugate (LC3-II), the cell death of both cells was categorized to achieve autophagy. Interestingly, an increase in cleaved-poly ADP ribose polymerase (cleaved-PARP) also showed the existence of an apoptosis-sensitive subpopulation. In both Dox-S and Dox-R cells, PI3K-p85/Akt/mTOR signaling pathways were reduced, which inhibited autophagy initiation. However, Beclin-1/PI3K-Class III downregulation implicated non-canonical autophagy pathways were involved in PG-induced autophagy. At completion of the PG regimen, tumors accumulated in the mice trachea and were attenuated by PG treatment, which indicated the efficacy of PG for both Dox-S and Dox-R lung cancer. All the above results concluded that PG is a potential chemotherapeutic agent for lung cancer regimens regardless of doxorubicin resistance.

A Comparative Study of the PD-L1 IHC 22C3 and 28-8 Assays on Lung Cancer Samples

2019 ◽  
Vol 104 (1) ◽  
pp. 236-237
Author(s):  
G.S. Krigsfeld ◽  
K. Zerba ◽  
J. Novotny ◽  
V. Chizhevsky ◽  
J.W. Ragheb ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Comparative Study

scholarly journals OA03.02 Nationwide Comparative Study Of PD-L1 IHC Assays on Lung Cancer: Initial Report Of LC-SCRUM-IBIS Project

2018 ◽  
Vol 13 (10) ◽  
pp. S324-S325
Author(s):  
N. Motoi ◽  
G. Ishii ◽  
Y. Hayashi ◽  
K. Tsuta ◽  
K. Yoh ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Comparative Study ◽  
Initial Report

scholarly journals Evodiamine suppresses non-small cell lung cancer by elevating CD8+ T cells and downregulating the MUC1-C/PD-L1 axis

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Ze-Bo Jiang ◽  
Ju-Min Huang ◽  
Ya-Jia Xie ◽  
Yi- Zhong Zhang ◽  
Chan Chang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
T Cells ◽  
Lewis Lung Carcinoma ◽  
Small Cell ◽  
Lewis Lung ◽  
Small Cell Lung ◽  
Programmed Death ◽  
Lewis Lung Carcinoma Model ◽  
Anti Tumor Activity

Abstract Background Accumulating evidence showed that regulating tumor microenvironment plays a vital role in improving antitumor efficiency. Programmed Death Ligand 1 (PD-L1) is expressed in many cancer cell types, while its binding partner Programmed Death 1 (PD1) is expressed in activated T cells and antigen-presenting cells. Whereas, its dysregulation in the microenvironment is poorly understood. In the present study, we confirmed that evodiamine downregulates MUC1-C, resulting in modulating PD-L1 expression in non-small cell lung cancer (NSCLC). Methods Cell viability was measured by MTT assays. Apoptosis, cell cycle and surface PD-L1 expression on NSCLC cells were analyzed by flow cytometry. The expression of MUC1-C and PD-L1 mRNA was measured by real time RT-PCR methods. Protein expression was examined in evodiamine-treated NSCLC cells using immunoblotting or immunofluorescence assays. The effects of evodiamine treatment on NSCLC sensitivity towards T cells were investigated using human peripheral blood mononuclear cells and Jurkat, apoptosis and IL-2 secretion assays. Female H1975 xenograft nude mice were used to assess the effect of evodiamine on tumorigenesis in vivo. Lewis lung carcinoma model was used to investigate the therapeutic effects of combination evodiamine and anti-PD-1 treatment. Results We showed that evodiamine significantly inhibited growth, induced apoptosis and cell cycle arrest at G2 phase of NSCLC cells. Evodiamine suppressed IFN-γ-induced PD-L1 expression in H1975 and H1650. MUC1-C mRNA and protein expression were decreased by evodiamine in NSCLC cells as well. Evodiamine could downregulate the PD-L1 expression and diminish the apoptosis of T cells. It inhibited MUC1-C expression and potentiated CD8+ T cell effector function. Meanwhile, evodiamine showed good anti-tumor activity in H1975 tumor xenograft, which reduced tumor size. Evodiamine exhibited anti-tumor activity by elevation of CD8+ T cells in vivo in Lewis lung carcinoma model. Combination evodiamine and anti-PD-1 mAb treatment enhanced tumor growth control and survival of mice. Conclusions Evodiamine can suppress NSCLC by elevating of CD8+ T cells and downregulating of the MUC1-C/PD-L1 axis. Our findings uncover a novel mechanism of action of evodiamine and indicate that evodiamine represents a potential targeted agent suitable to be combined with immunotherapeutic approaches to treat NSCLC cancer patients. MUC1-C overexpression is common in female, non-smoker, patients with advanced-stage adenocarcinoma.

Sulfated galactofucan from Sargassum thunbergii induces senescence in human lung cancer A549 cells

2020 ◽  
Vol 11 (5) ◽  
pp. 4785-4792
Author(s):  
Yizhong Bao ◽  
Xinyue He ◽  
Wanli Wu ◽  
Sanying Wang ◽  
Jihuan Dai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cell ◽  
Human Lung ◽  
A549 Cells ◽  
Cell Senescence ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Sargassum Thunbergii

Our data indicated that a sulfated galactofucan (SWZ-4-H) from Sargassum thunbergii could induce lung cancer cell senescence by regulating p53, p21, p16, and p-Rb.

Sign in / Sign up

Export Citation Format

Share Document