scholarly journals α-Catulin promotes cancer stemness by antagonizing WWP1-mediated KLF5 degradation in lung cancer

Theranostics ◽  
2022 ◽  
Vol 12 (3) ◽  
pp. 1173-1186
Author(s):  
Chia-Hao Tung ◽  
Meng-Fan Huang ◽  
Chen-Hsien Liang ◽  
Yi-Ying Wu ◽  
Jia-En Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Stemness

Abstract 1052: Stearoyl-CoA-Desaturase (SCD1) regulates lung cancer stemness via stabilization and nuclear localization of YAP/TAZ

2016 ◽  
Author(s):  
Alessia Noto ◽  
Maria Elena Pisanu ◽  
Claudia De Vitis ◽  
Giovanni Sorrentino ◽  
Giannino Del Sal ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Nuclear Localization ◽  
Cancer Stemness ◽  
Stearoyl Coa Desaturase

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.

A phase Ib/II study of cancer stemness inhibitor napabucasin (BB608) combined with weekly paclitaxel in advanced non-small cell lung cancer.

2016 ◽  
Vol 34 (15_suppl) ◽  
pp. 9093-9093 ◽  
Author(s):  
Carlos Becerra ◽  
Alexander I. Spira ◽  
Paul R. Conkling ◽  
Stephen Lane Richey ◽  
Wahid Tewfik Hanna ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Weekly Paclitaxel ◽  
Small Cell Lung ◽  
Cancer Stemness ◽  
Phase Ib

scholarly journals Targeting BMI1 and MCL1 for Lung Adenocarcinoma Treatment

2018 ◽  
Author(s):  
Erh-Hsuan Lin ◽  
Chiung-Fang Hsu ◽  
Yi-Hua Jan ◽  
Tsung-Hsien Lin ◽  
Hsiang-Yi Chang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Tumor Formation ◽  
Poor Survival ◽  
Cancer Stemness ◽  
Jnk Signaling ◽  
Chemotherapy Agent ◽  
Potential Strategy ◽  
Environment Stress ◽  
High Level

AbstractLung cancer is the leading cause of cancer-associated death worldwide. Early metastasis and the recurrence remain major challenges for lung cancer treatment in clinic. Targeting the cancer stemness could be a potential strategy to restrain tumor progression. In the current study, we found that in lung adenocarcinoma (LAC), BMI1 and MCL1 play crucial roles in invasion, chemo-resistance, and tumor initiation. JNK signaling is a link between oncogenic pathway or environment stress to cancer stemness. The activation of JNK, either by EGFR or chemotherapy agent, stabilized BMI1 and MCL1 proteins through suppressing the expression of E3-ubiquitin ligase HUWE1. In lung cancer patient samples, high level of BMI1 is correlated with poor survival, and the expression of BMI1 is positively correlated with MCL1. A novel small-molecule BI-44 was synthesized, which effectively suppressed BMI1/MCL1 expression and inhibited tumor formation and progression in preclinical models. Targeting BMI1/MCL1 provides the basis for a new therapeutic approach in the treatment of LAC.

scholarly journals IL‐10 derived from M2 macrophage promotes cancer stemness via JAK1/STAT1/NF‐κB/Notch1 pathway in non‐small cell lung cancer

2019 ◽  
Vol 145 (4) ◽  
pp. 1099-1110 ◽  
Author(s):  
Li Yang ◽  
Ying Dong ◽  
Yanjun Li ◽  
Dong Wang ◽  
Shasha Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
M2 Macrophage ◽  
Small Cell Lung ◽  
Cancer Stemness

scholarly journals Rab37 mediates exocytosis of secreted frizzled-related protein 1 to inhibit Wnt signaling and thus suppress lung cancer stemness

2018 ◽  
Vol 9 (9) ◽  
Author(s):  
Shu-Huei Cho ◽  
I-Ying Kuo ◽  
Pei-Jung Frank Lu ◽  
Hong-Tai Tzeng ◽  
Wu-Wei Lai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Wnt Signaling ◽  
Related Protein ◽  
Cancer Stemness

Ubiquitin-protein ligase E3C maintains non-small-cell lung cancer stemness by targeting AHNAK-p53 complex

2019 ◽  
Vol 443 ◽  
pp. 125-134 ◽  
Author(s):  
Jie Gu ◽  
Wei Mao ◽  
Wenjia Ren ◽  
Fengkai Xu ◽  
Qiaoliang Zhu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cancer Stemness ◽  
Ubiquitin Protein Ligase

scholarly journals EGFR-AS1/HIF2A regulates the expression of FOXP3 to impact the cancer stemness of smoking-related non-small cell lung cancer

2019 ◽  
Vol 11 ◽  
pp. 175883591985522 ◽  
Author(s):  
Haolong Qi ◽  
Shanshan Wang ◽  
Juekun Wu ◽  
Shucai Yang ◽  
Steven Gray ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cell ◽  
Cell Lung Cancer ◽  
Foxp3 Expression ◽  
Small Cell ◽  
Nsclc Cell ◽  
Lung Cancer Cell ◽  
Small Cell Lung ◽  
Cancer Stemness

Background: Early data showed that FOXP3 could induce epithelial-mesenchymal transition by stimulating the Wnt/β-catenin signaling pathway in non-small cell lung cancer (NSCLC). However, how the expression of FOXP3 is regulated in NSCLC remains unknown. We thus explored the impacts of the long noncoding RNA EGFR antisense RNA 1 (EGFR-AS1) and hypoxia-inducible factor-2A (HIF2A) on FOXP3 expression and the cancer stemness of NSCLC. Methods: Lung tissues samples from 87 patients with NSCLC and two NSCLC cell lines were used in this study. The regulation of FOXP3 and lung cancer cell stemness by EGFR-AS1 and HIF2A was determined at molecular levels in NSCLC tissue samples and cultured cells in the presence/absence of the smoking carcinogen, 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (also known as nicotine-derived nitrosamine ketone). The results were confirmed in tumor xenograft models. Results: We found that NNK decreased the expression of EGFR-AS1 in the long term, but increased the expression of HIF2A and FOXP3 to stimulate lung cancer cell stemness. EGFR-AS1 significantly inhibited FOXP3 expression and NSCLC cell stemness, whereas HIF2A obviously promoted both. The enhancement of lung cancer stemness by FOXP3 was, at least partially, via stimulating Notch1, as the inhibition of Notch1 could markedly diminish the effect of FOXP3. Conclusions: FOXP3, the expression of which is under the fine control of EGFR-AS1, is a critical molecule that promotes NSCLC cancer cell stemness through stimulating the Notch1 pathway.

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