scholarly journals Roles of nitric oxide on cancer stemness and metastasis in lung cancer cells

2016 ◽  
Vol 11 (1) ◽  
pp. 24-25 ◽  
Author(s):  
Pithi Chanvorachote ◽  
Varisa Pongrakhananon ◽  
Chatchai Chaotham
Keyword(s):  
Nitric Oxide ◽  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Cancer Stemness

scholarly journals Combination of Sasa quelpaertensis Nakai Leaf Extract and Cisplatin Suppresses the Cancer Stemness and Invasion of Human Lung Cancer Cells

2014 ◽  
Vol 13 (6) ◽  
pp. 529-540 ◽  
Author(s):  
Mina Kim ◽  
Yoo-Sun Kim ◽  
Kyung-Mi Kim ◽  
Hee-Chul Ko ◽  
Se-Jae Kim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Stem Cell Markers ◽  
Cancer Stemness ◽  
Human Lung Cancer Cells

Lung cancer is the leading cause of cancer death worldwide, and most chemotherapeutic drugs have limited success in treating this disease. Furthermore, some drugs show undesirable side effects due to the enrichment of cancer stem cells (CSCs) that are present, leading to resistance to conventional chemotherapy and tumor relapse. CSCs possess self-renewal characteristics, aggressive tumor initiating activity, and ability to facilitate tumor metastasis. Therefore, development of nontoxic agents that can potentiate chemotherapy and eliminate CSCs would be highly desirable. In the present study, we investigated whether Sasa quelpaertensis leaf extracts (SQE) and cisplatin (CIS), individually or in combination, would exert anti-CSC and antimetastatic effect in H1299 and A549 human lung cancer cells. Following these treatments, cell growth, phosphorylation of phosphoinositide-3 kinase, and activation of the mammalian target of rapamycin were inhibited. Decreased serial sphere formation, clonogenicity, and expression of major stem cell markers, such as CD44 and SOX-2, in CD44+ cancer stem cells were also observed. In addition, inhibition of cell migration and invasion in both cell lines as well as inhibition of matrix metalloproteinase-2 activity and expression were detected. Importantly, the anticancer stemness and antimetastasis effects in each of these assays were greater for the combined treatment with SQE and CIS than with each treatment individually. In conclusion, the data suggest that SQE alone, or in combination with CIS, represents a promising therapeutic strategy for eliminating cancer stemness and cell invasion potential of CSCs, thereby treating and preventing metastatic lung cancer cells.

scholarly journals Long-Term Nitric Oxide Exposure Enhances Lung Cancer Cell Migration

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Arpasinee Sanuphan ◽  
Preedakorn Chunhacha ◽  
Varisa Pongrakhananon ◽  
Pithi Chanvorachote
Keyword(s):  
Nitric Oxide ◽  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Biology ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Dependent Manner

Nitric oxide (NO) found in the vicinity of lung cancer cells may play a role in the regulation of cancer cell behaviors. To explore the possible effects of NO on cell motility, human lung cancer cells were exposed to nontoxic concentrations of NO for 0–14 days, and the migratory characteristics of the cells were determined. The present study found that long-term treatment with NO significantly enhanced cell migration in a dose- and time-dependent manner. Furthermore, we found that the increased migratory action was associated with the increased expression of caveolin-1 (Cav-1), which in turn activated the focal adhesion kinase (FAK) and ATP-dependent tyrosine kinase (Akt) pathways. Notably, the NO-treated cells exhibited an increased number of filopodia per cell, as well as an increase in the levels of cell division cycle 42 (Cdc42) protein. Together, these results indicate that extended NO exposure has a novel effect on cell migration through a Cav-1-dependent mechanism, a finding that strengthens our understanding of cancer biology.

FGF1 and IGF1-conditioned 3D culture system promoted the amplification and cancer stemness of lung cancer cells

Biomaterials ◽  
2017 ◽  
Vol 149 ◽  
pp. 63-76 ◽  
Author(s):  
Pengpeng Liu ◽  
Rui Zhang ◽  
Wenwen Yu ◽  
Yingnan Ye ◽  
Yanan Cheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Culture System ◽  
3D Culture ◽  
Lung Cancer Cells ◽  
Cancer Stemness ◽  
3D Culture System

scholarly journals Mycelial Extract ofPhellinus linteusInduces Cell Death in A549 Lung Cancer Cells and Elevation of Nitric Oxide in Raw 264.7 Macrophage Cells

Mycobiology ◽  
2006 ◽  
Vol 34 (3) ◽  
pp. 143 ◽  
Author(s):  
Jong-Jin Lee ◽  
Ho-Kyun Kwon ◽  
Dong-Soo Lee ◽  
Seung-Woo Lee ◽  
Kye-Kwan Lee ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Raw 264.7 ◽  
Macrophage Cells ◽  
Mycelial Extract ◽  
Raw 264.7 Macrophage Cells ◽  
A549 Lung

scholarly journals CD44 Promotes Lung Cancer Cell Metastasis through ERK–ZEB1 Signaling

Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 4057
Author(s):  
Yen-Yun Wang ◽  
Anupama Vadhan ◽  
Ping-Ho Chen ◽  
Yen-Lung Lee ◽  
Chih-Yeh Chao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lymph Nodes ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Cancer Stemness ◽  
Primary Tumors

Lung cancer is a malignancy with high mortality worldwide, and metastasis occurs at a high frequency even when cancer spread is not detectable at primary operation. Cancer stemness plays an important role in malignant cancer behavior, treatment resistance, and cancer metastasis. Therefore, understanding the molecular pathogenesis behind cancer-stemness-mediated metastasis and developing effective approaches to prevent metastasis are key issues for improving cancer treatment. In this study, we investigated the role of CD44 stemness marker in lung cancer using in vitro and clinical studies. Immunohistochemical staining of lung cancer tissue specimens revealed that primary tumors with higher CD44 expression showed increased metastasis to regional lymph nodes. Flow cytometry analysis suggested that CD44 positive cells were enriched in the metastatic lymph nodes compared to the primary tumors. CD44 overexpression significantly increased migration and invasion abilities of lung cancer cells through CD44-induced ERK phosphorylation, ZEB1 upregulation, and Claudin-1 downregulation. Furthermore, ERK inhibition suppressed the migration and invasion abilities of CD44-overexpressing lung cancer cells. In summary, our in vitro and clinical results indicate that CD44 may be a potential prognostic and therapeutic marker for lung cancer patients.

scholarly journals L-Type Amino Acid Transporter 1 Regulates Cancer Stemness and the Expression of Programmed Cell Death 1 Ligand 1 in Lung Cancer Cells

2021 ◽  
Vol 22 (20) ◽  
pp. 10955
Author(s):  
Yi-Heng Liu ◽  
Yu-Ling Li ◽  
Huan-Ting Shen ◽  
Peng-Ju Chien ◽  
Gwo-Tarng Sheu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Amino Acid ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Amino Acid Transporter ◽  
Lung Cancer Cells ◽  
Cancer Stemness ◽  
Programmed Cell Death 1 ◽  
Acid Transporter

The l-type amino acid transporter 1 (LAT1) is a membranous transporter that transports neutral amino acids for cells and is dysregulated in various types of cancer. Here, we first observed increased LAT1 expression in pemetrexed-resistant non-small cell lung cancer (NSCLC) cells with high cancer stem cell (CSC) activity, and its mRNA expression level was associated with shorter overall survival in the lung adenocarcinoma dataset of the Cancer Genome Atlas database. The inhibition of LAT1 by a small molecule inhibitor, JPH203, or by RNA interference led to a significant reduction in tumorsphere formation and the downregulation of several cancer stemness genes in NSCLC cells through decreased AKT serine/threonine kinase (AKT)/mammalian target of rapamycin (mTOR) activation. The treatment of the cell-permeable leucine derivative promoted AKT/mTOR phosphorylation and reversed the inhibitory effect of JPH203 in the reduction of CSC activity in pemetrexed-resistant lung cancer cells. Furthermore, we observed that LAT1 silencing caused the downregulation of programmed cell death 1 ligand 1 (PD-L1) on lung cancer cells. The PD-L1+/LAT1+ subpopulation of NSCLC cells displayed great CSC activity with increased expression of several cancer stemness genes. These data suggest that LAT1 inhibitors can serve as anti-CSC agents and could be used in combination with immune checkpoint inhibitors in lung cancer therapy.

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