scholarly journals Correction: microRNA-let-7e in serum-derived exosomes inhibits the metastasis of non-small-cell lung cancer in a SUV39H2/LSD1/CDH1-dependent manner

2021 ◽  
Author(s):  
Shufeng Xu ◽  
Lei Zheng ◽  
Liying Kang ◽  
Hongmei Xu ◽  
Liming Gao
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Dependent Manner ◽  
Small Cell Lung

scholarly journals Silibinin Regulates Tumor Progression and Tumorsphere Formation by Suppressing PD-L1 Expression in Non-Small Cell Lung Cancer (NSCLC) Cells

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1632
Author(s):  
Alexis Rugamba ◽  
Dong Young Kang ◽  
Nipin Sp ◽  
Eun Seong Jo ◽  
Jin-Moo Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Small Cell Lung Cancer ◽  
Anticancer Activity ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Molecular Signaling ◽  
Small Cell Lung

Recently, natural compounds have been used globally for cancer treatment studies. Silibinin is a natural compound extracted from Silybum marianum (milk thistle), which has been suggested as an anticancer drug through various studies. Studies on its activity in various cancers are undergoing. This study demonstrated the molecular signaling behind the anticancer activity of silibinin in non-small cell lung cancer (NSCLC). Quantitative real-time polymerase chain reaction and Western blotting analysis were performed for molecular signaling analysis. Wound healing assay, invasion assay, and in vitro angiogenesis were performed for the anticancer activity of silibinin. The results indicated that silibinin inhibited A549, H292, and H460 cell proliferation in a concentration-dependent manner, as confirmed by the induction of G0/G1 cell cycle arrest and apoptosis and the inhibition of tumor angiogenesis, migration, and invasion. This study also assessed the role of silibinin in suppressing tumorsphere formation using the tumorsphere formation assay. By binding to the epidermal growth factor receptor (EGFR), silibinin downregulated phosphorylated EGFR expression, which then inhibited its downstream targets, the JAK2/STAT5 and PI3K/AKT pathways, and thereby reduced matrix metalloproteinase, PD-L1, and vascular endothelial growth factor expression. Binding analysis demonstrated that STAT5 binds to the PD-L1 promoter region in the nucleus and silibinin inhibited the STAT5/PD-L1 complex. Altogether, silibinin could be considered as a candidate for tumor immunotherapy and cancer stem cell-targeted therapy.

scholarly journals Micheliolide Enhances Radiosensitivities of p53-Deficient Non-Small-Cell Lung Cancer via Promoting HIF-1α Degradation

2020 ◽  
Vol 21 (9) ◽  
pp. 3392
Author(s):  
Peizhong Kong ◽  
K.N. Yu ◽  
Miaomiao Yang ◽  
Waleed Abdelbagi Almahi ◽  
Lili Nie ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Hypoxic Exposure ◽  
Dependent Manner ◽  
Wild Type ◽  
Small Cell Lung ◽  
H460 Cells ◽  
Wild Type P53

Micheliolide (MCL) has shown promising anti-inflammatory and anti-tumor efficacy. However, whether and how MCL enhances the sensitivity of non-small-cell lung cancer (NSCLC) to radiotherapy are still unknown. In the present paper, we found that MCL exerted a tumor cell killing effect on NSCLC cells in a dose-dependent manner, and MCL strongly sensitized p53-deficient NSCLC cells, but not the cells with wild-type p53 to irradiation (IR). Meanwhile, MCL markedly inhibited the expression of hypoxia-inducible factor-1α (HIF-1α) after IR and hypoxic exposure in H1299 and Calu-1 cells rather than in H460 cells. Consistently, radiation- or hypoxia-induced expression of vascular endothelial growth factor (VEGF) was also significantly inhibited by MCL in H1299 and Calu-1 cells, but not in H460 cells. Therefore, inhibition of the HIF-1α pathway might, at least in part, contribute to the radiosensitizing effect of MCL. Further study showed that MCL could accelerate the degradation of HIF-1α through the ubiquitin-proteosome system. In addition, the transfection of wild-type p53 into p53-null cells (H1299) attenuated the effect of MCL on inhibiting HIF-1α expression. These results suggest MCL effectively sensitizes p53-deficient NSCLC cells to IR in a manner of inhibiting the HIF-1α pathway via promoting HIF-1α degradation, and p53 played a negative role in MCL-induced HIF-1α degradation.

scholarly journals Antitumor Effect of Membrane-type PBLs on Non-Small Cell Lung Cancer Cell of ICR Mice

2020 ◽  
Author(s):  
Junli Cao ◽  
Peng Su ◽  
Yuefeng Zhang ◽  
Xin Wang ◽  
Xiwei Lu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Synergistic Effect ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Time Dependent ◽  
Control Group ◽  
Dependent Manner ◽  
Small Cell Lung ◽  
Icr Mice

Abstract This study aims at probing the inhibitory effect of transmembrane PBLs on non-small cell lung cancer (NSCLC) H446 cells and the potential application of PBLs on immune system of the experimental mice loaded with H446 cells. The changes of the gene expression of microRNA-25 and 223 in ICR mice with NSCLC were also investigated. Sixty ICR mice were randomly divided into experimental and control groups. The animal model was established via inoculation of NSCLC H446 cells at the hind thigh of mice. The plasmid PBLs was dissolved in saline solution and injected into the muscle of left thigh of the mice in experimental groups with different doses (0.1 mg, 0.2 mg and 0.3 mg per ICR mouse) using in situ injection method. After injection of PBLs solution, each three mice were killed at 12 h, 24 h, 36 h, and 48 h, respectively. The expression of microRNA-25 and 223 were detected by semi-quantitative reverse transcription-polymerase chain reaction. Tumor Necrosis Factor-γ (TNF-γ), Interleukelin-2 (IL-2) and Heat Shock Protein 70 (HSP70) in Bronchoalveolar Lavage Fluid (BALF) were detected by enzyme-linked immunosorbent assay. The expression of TNF-γ and IL-2 protein in lung tissue were detected by western blotting. The expression of microRNA-25 was up-regulated in the tissues and BALF with a dose- and time-dependent manner while microRNA-223 was down-regulated. The difference were statistically significant comparing the control group (P<0.05). The TNF-γ and IL-2 levels in BALF of ICR mice in experimental group were increased comparing the control group with a dose-dependent manner (P<0.05). Synergistic effect between PBLs and HSP70 was also studied. It was found that the growth of tumor was significantly suppressed after the transfection of PBLs. In the presence of PBLs, the proliferation of splenocytes and cytolysis in early phase of tumor development was significantly enhanced. Thus, such anti-tumor effect was further improved by the synergistic effect of PBLs with HSP70. The expression of microRNA-25 and 223 are associated with NSCLC in a dose- and time-dependent manner, they might be considered as potential biomarkers for early diagnosis of NSCLC.

scholarly journals Telomerase inhibitor imetelstat has preclinical activity across the spectrum of non-small cell lung cancer oncogenotypes in a telomere length dependent manner

Oncotarget ◽  
2016 ◽  
Vol 7 (22) ◽  
pp. 31639-31651 ◽  
Author(s):  
Robin E. Frink ◽  
Michael Peyton ◽  
Joan H. Schiller ◽  
Adi F. Gazdar ◽  
Jerry W. Shay ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Telomere Length ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Dependent Manner ◽  
Small Cell Lung ◽  
Telomerase Inhibitor

scholarly journals Analysis of Long Noncoding RNAs in Aila-Induced Non-Small Cell Lung Cancer Inhibition

2021 ◽  
Vol 11 ◽  
Author(s):  
Lin Chen ◽  
Cui Wu ◽  
Heming Wang ◽  
Sinuo Chen ◽  
Danhui Ma ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Early Stage ◽  
Noncoding Rnas ◽  
Small Cell ◽  
Long Noncoding Rnas ◽  
Dependent Manner ◽  
Small Cell Lung ◽  
Cancer Inhibition

Non-small cell lung cancer (NSCLC) has the highest morbidity and mortality among all carcinomas. However, it is difficult to diagnose in the early stage, and current therapeutic efficacy is not ideal. Although numerous studies have revealed that Ailanthone (Aila), a natural product, can inhibit multiple cancers by reducing cell proliferation and invasion and inducing apoptosis, the mechanism by which Aila represses NSCLC progression in a time-dependent manner remains unclear. In this study, we observed that most long noncoding RNAs (lncRNAs) were either notably up- or downregulated in NSCLC cells after treatment with Aila. Moreover, alterations in lncRNA expression induced by Aila were crucial for the initiation and metastasis of NSCLC. Furthermore, in our research, expression of DUXAP8 was significantly downregulated in NSCLC cells after treatment with Aila and regulated expression levels of EGR1. In conclusion, our findings demonstrate that Aila is a potent natural suppressor of NSCLC by modulating expression of DUXAP8 and EGR1.

scholarly journals A dose- and time-dependent effect of oxythiamine on cell growth inhibition in non-small cell lung cancer

2021 ◽  
Author(s):  
Lin Bai ◽  
Hui-li Zhu
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Critical Role ◽  
A549 Cells ◽  
Small Cell ◽  
Time Dependent ◽  
Dependent Manner ◽  
Small Cell Lung

AbstractThe high mortality rate of non-small-cell lung cancer (NSCLC) is mostly due to the high risk of recurrence. A comprehensive understanding of proliferation mechanisms of NSCLC would remarkably contribute to blocking up the invasion and metastasis of tumor cells. In our previous study, the remarkable decreased activity of Thiamine-dependent enzymes (TDEs), involving in intermediary metabolism responsible for energy production of tumor, was found under conditions of thiamine deficiency in vivo. To explore the effect of Oxythiamine (OT), a TDEs antimetabolite, on cell growth, we co-cultured A549 cells with OT in vitro at various doses (0.1, 1, 10 and 100 μM) and time periods (6, 12, 24 and 48 h) and subsequent cell proliferation and apoptosis assays were performed respectively. Our findings demonstrated that A549 cells proliferation was significantly downregulated by OT treatment in a progressively dose as well as time dependent manner. Inhibition of TDEs resulted in antagonism of lung cancer growth by inducing cells to cease the cycle as well as apoptotic cell death. We concluded a critical role of OT, a TDEs antagonistic compound, indicating the potential target of its practical use.

scholarly journals KRASQ61H preferentially signals through MAPK in a RAF dimer-dependent manner in non-small cell lung cancer

2020 ◽  
pp. canres.0448.2020
Author(s):  
Zhi-Wei Zhou ◽  
Chiara Ambrogio ◽  
Asim K Bera ◽  
Qing Li ◽  
Xing-Xiao Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Dependent Manner ◽  
Small Cell Lung

Effect of metformin on the effects of TKI on human lung carcinoma cells harboring KRAS or EGFR-T790M mutation.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e18051-e18051
Author(s):  
Yongsheng Wang ◽  
Yu Ma ◽  
Dan Li ◽  
Fuchun Guo
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Dependent Manner ◽  
Small Cell Lung ◽  
T790m Mutation ◽  
Tki Resistance ◽  
Egfr Tki ◽  
Egfr T790m

e18051 Background: K-ras and egfr-T790M mutation show primary and acquired resistance to EGFR-TKI in non-small cell lung cancer, respectively. The antidiabetic drug metformin has been associated with a decreased incidence and a better prognosis of lung cancer. The affects of metformin on the EGFR-TKI resistance in non-small cell lung cancer remain unknown. Methods: The effects of metformin on EGFR-TKI were investigated in k-ras mutant A549 cells, and egfr-T790M mutant H1975 cells both in virto and in vivo. The proliferation and apoptosis were tested. The underlying mechanisms were also analyzed. Results: Our data showed metformin significantly enhanced the inhibition activity of gefitinib both in A549 and H1975 cells in vitro. At the molecular level, metformin inhibited multiple signaling including LKB1-AMPK-S6K, PI3K-AKT and Raf-MEK-MAPK in a dose-dependent manner. Furthermore, the increased tumor inhibitions were observed in nude mice models of A549 (P<0.05)and H1975 (P<0.01). Conclusions: Metformin can increase the effects of EGFR-TKI in lung adenocarcinoma harboring K-ras and egfr-T790M mutation. Our study may provide a new strategy to overcome the EGFR-TKI resistance in NSCLC.

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