scholarly journals Se-Enriched Cordyceps militaris Inhibits Cell Proliferation, Induces Cell Apoptosis, And Causes G2/M Phase Arrest In Human Non-Small Cell Lung Cancer Cells

2019 ◽  
Vol Volume 12 ◽  
pp. 8751-8763 ◽  
Author(s):  
Lihua Luo ◽  
Ruizhi Ran ◽  
Jie Yao ◽  
Fang Zhang ◽  
Maohui Xing ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Phase Arrest ◽  
M Phase

scholarly journals MiR-222-3p Promotes Cell Proliferation and Inhibits Apoptosis by Targeting PUMA (BBC3) in Non-Small Cell Lung Cancer

2020 ◽  
Vol 19 ◽  
pp. 153303382092255
Author(s):  
Weijun Chen ◽  
Xiaobo Li
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Binding Component

MicroRNAs have been demonstrated to be critical regulators in tumor progression, including non-small cell lung cancer. MicroRNA-222-3p has been reported to function as a tumor suppressor or oncogene in several types of cancer, but its function role in non-small cell lung cancer has not been uncovered. In this study, we first found the expression of microRNA-222-3p was significantly increased in non-small cell lung cancer tissues and cell lines. MicroRNA-222-3p inhibitor decreased the activity of non-small cell lung cancer cells to proliferate and increased cell apoptosis using cell counting kit-8, flow cytometry, and caspase-3 activity analysis. Overexpressed microRNA-222-3p in non-small cell lung cancer cells promoted cell proliferation, but decreased cell apoptosis. Moreover, Bcl-2-binding component 3 was the target gene of microRNA-222-3p, and its knockdown weakened the regulatory effect of microRNA-222-3p inhibitor on cell proliferation and apoptosis in non-small cell lung cancer cells. In conclusion, microRNA-222-3p plays a significant role in the regulation of Bcl-2-binding component 3 expression and might be a promising target for clinical non-small cell lung cancer therapy.

scholarly journals XQ2, a Novel TPZ Derivative, Induced G2/M Phase Arrest and Apoptosis under Hypoxia in Non-Small Cell Lung Cancer Cells

2010 ◽  
Vol 74 (6) ◽  
pp. 1181-1187 ◽  
Author(s):  
Jianshu LOU ◽  
XingLu ZHOU ◽  
Qinjie WENG ◽  
Duo-duo WANG ◽  
Qing XIA ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Phase Arrest ◽  
M Phase

scholarly journals Midazolam increases cisplatin-sensitivity in non-small cell lung cancer (NSCLC) via the miR-194-5p/HOOK3 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tingting Sun ◽  
Jing Chen ◽  
Xuechao Sun ◽  
Guonian Wang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Cisplatin Resistance ◽  
Small Cell ◽  
Luciferase Reporter ◽  
Small Cell Lung ◽  
Cisplatin Sensitivity

Abstract Backgrounds As previously reported, midazolam anesthesia exerts tumor-suppressing effects in non-small cell lung cancer (NSCLC), but the regulating effects of this drug on cisplatin-resistance in NSCLC have not been studied. Thus, we designed this study to investigate this issue and preliminarily delineate the potential molecular mechanisms. Methods We performed MTT assay and trypan blue staining assay to measure cell proliferation and viability. Cell apoptosis was examined by FCM. qRT-PCR and immunoblotting were performed to determine the expression levels of genes. The targeting sites between genes were predicted by bioinformatics analysis and were validated by dual-luciferase reporter gene system assay. Mice tumor-bearing models were established and the tumorigenesis was evaluated by measuring tumor weight and volume. Immunohistochemistry (IHC) was used to examine the pro-proliferative Ki67 protein expressions in mice tumor tissues. Results The cisplatin-resistant NSCLC (CR-NSCLC) cells were treated with high-dose cisplatin (50 μg/ml) and low-dose midazolam (10 μg/ml), and the results showed that midazolam suppressed cell proliferation and viability, and promoted cell apoptosis in cisplatin-treated CR-NSCLC cells. In addition, midazolam enhanced cisplatin-sensitivity in CR-NSCLC cell via modulating the miR-194-5p/hook microtubule-tethering protein 3 (HOOK3) axis. Specifically, midazolam upregulated miR-194-5p, but downregulated HOOK3 in the CR-NSCLC cells, and further results validated that miR-194-5p bound to the 3’ untranslated region (3’UTR) of HOOK3 mRNA for its inhibition. Also, midazolam downregulated HOOK3 in CR-NSCLC cells by upregulating miR-194-5p. Functional experiments validated that both miR-194-5p downregulation and HOOK3 upregulation abrogated the promoting effects of midazolam on cisplatin-sensitivity in CR-NSCLC cells. Conclusions Taken together, this study found that midazolam anesthesia reduced cisplatin-resistance in CR-NSCLC cells by regulating the miR-194-5p/HOOK3 axis, implying that midazolam could be used as adjuvant drug for NSCLC treatment in clinical practices.

scholarly journals Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells

2018 ◽  
Vol 13 ◽  
pp. 334-346 ◽  
Author(s):  
Valentina Russo ◽  
Alessia Paciocco ◽  
Alessandra Affinito ◽  
Giuseppina Roscigno ◽  
Danilo Fiore ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung

scholarly journals High levels of MESP1 expression in non-small cell lung cancer can facilitate cell proliferation, metastasis and suppresses cell apoptosis

2020 ◽  
Vol 9 (10) ◽  
pp. 5956-5968
Author(s):  
Lei Wang ◽  
Chunyan Yang ◽  
Fangfang Li ◽  
Dengcai Mu ◽  
Pengzhan Ran ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Small Cell ◽  
Small Cell Lung

Effects of miR-1305 on Proliferation and Apoptosis of Non-Small Cell Lung Cancer Cells via Regulating High Mobility Group Box-1 Level

2020 ◽  
Vol 10 (12) ◽  
pp. 1837-1842
Author(s):  
Wenpu Zhao ◽  
Xiaolian Yang ◽  
Yishan Dong ◽  
Jin Quan ◽  
Li Huang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Mrna Level ◽  
Small Cell ◽  
Small Cell Lung ◽  
Hmgb1 Level ◽  
Proliferation And Apoptosis

Abnormal expression of HMGB1 is closely related to non-small cell lung cancer (NSCLC). miR-1305 regulates HMGB1 level by MiRDB analysis. Therefore, we investigated whether miR-1305 affects NSCLC cell proliferation and apoptosis by regulating HMGB1. The control group (NC group), miR-1305 Mimics group and miR-1305 Mimics+pcDNA-HMGB1 group were set followed by analysis of miR-1305 and HMGB1 mRNA level real time-PCR, relationship between miR-1305 and HMGB1 by dual fluorescein reporter assay, HMGB1 and Tubulin level by Western blot, cell proliferation by clone formation assay, cell apoptosis by Annexin V-FITC/PI staining. Compared with normal tissues, miR-1305 was significantly downregulated in NSCLC tissues (P <0.01), while HMGB1 mRNA was upregulated (P <0.01). HMGB1 was the target gene of miR-1305. Compared to NC group, HMGB1 level in miR-1305 Mimics group was significantly reduced (P <0.01). Compared with miR-1305 Mimics group, HMGB1 level was significantly increased in miR-1305 Mimics+pcDNA-HMGB1group (P <0.05). HMGB1 mRNA level was not significantly changed. In addition, the number of cell clones and proliferation ability was decreased in miR-1305 Mimics group, which were reversed in miR-1305 Mimics+pcDNA-HMGB1 group. miR-1305 can bind HMGB1 3′-UTR, reduce its protein level, thereby inhibiting NSCLC cell proliferation and promoting cell apoptosis. HMGB1 overexpression can prevent the effect of miR-1305.

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