scholarly journals Ginsenoside Rh7 Suppresses Proliferation, Migration and Invasion of NSCLC Cells Through Targeting ILF3-AS1 Mediated miR-212/SMAD1 Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiangbo Chen ◽  
Wenguang Liu ◽  
Bao Liu
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Therapeutic Target ◽  
Bioinformatics Analysis ◽  
Small Cell ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Antitumor Effects ◽  
First Time

It is reported that ginsenosides have a significant anti-tumor effect on a variety of tumors. However, the role and mechanism of Rh7 in non-small cell lung cancer (NSCLC) are unclear. In this study, we aimed to study the anti-tumor effect of Rh7 on the proliferation and progression of NSCLC. Bioinformatics analysis showed that ILF3-AS1 was regulated by ginsenoside Rh7 in NSCLC. Down-regulation of ILF3-AS1 could significantly inhibit the proliferation, metastasis and invasion of NSCLC. In addition, ILF3-AS1 negatively controlled miR-212, which in turn targeted SMAD1 expression, thereby regulating NSCLC cell viability and apoptosis. Our results indicate that ILF3-AS1 can be used as a diagnostic and therapeutic target for non-small cell lung cancer. It is discovered for the first time that ginsenoside Rh7 inhibits the expression of ILF3-AS1 and exerts antitumor effects.

scholarly journals HAGLROS is overexpressed and promotes non-small cell lung cancer migration and invasion

2020 ◽  
Vol 50 (9) ◽  
pp. 1058-1067 ◽  
Author(s):  
Ying Chen ◽  
Tianle Shen ◽  
Xuping Ding ◽  
Lei Cheng ◽  
Liming Sheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Overall Survival ◽  
Small Cell Lung Cancer ◽  
Survival Time ◽  
Cell Lung Cancer ◽  
Bioinformatics Analysis ◽  
Small Cell ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Normal Tissues

Abstract Introduction Non-small cell lung cancer was one of the most common and deadly cancers worldwide. Long non-coding RNAs had been implicated in multiple human cancers, including non-small cell lung cancer. In this study, we focused on a novel long non-coding RNA, HAGLROS, in non-small cell lung cancer. Material and methods In this study, we used GEPIA dataset to analyse the expression levels of HAGLROS in non-small cell lung cancer samples and normal tissues. Then, we analysed Kaplan–Meier Plotter database to reveal the association between HAGLROS expression and overall survival time in patients with non-small cell lung cancer. Moreover, we used small interfering RNA-mediated knockdown to reduce HAGLROS expression in A549 and H1299 cells. Cell Counting Kit-8 assay was used to detect the effect of HAGLROS on cell proliferation. Transwell assays were used to determine the effect of HAGLROS on cell migration and invasion. Co-expression analysis and bioinformatics analysis were conducted to predict the potential functions of HAGLROS in non-small cell lung cancer. Results We identified HAGLROS was significantly overexpressed in non-small cell lung cancer samples compared to normal tissues. Higher expression of HAGLROS was significantly associated with shorter overall survival time in patients with non-small cell lung cancer. Moreover, we found knockdown of HAGLROS in non-small cell lung cancer cells remarkably suppressed tumour proliferation, migration and invasion. By conducting bioinformatics analysis, we found HAGLROS was involved in regulating multiple cancer-related pathways, including Spliceosome, DNA replication, cell cycle, chromosome segregation and sister chromatid segregation. Conclusions Our results for the first time demonstrated HAGLROS may serve as a target for new therapies in non-small cell lung cancer.

scholarly journals circ_0002346 Suppresses Non-Small-Cell Lung Cancer Progression Depending on the Regulation of the miR-582-3p/STXBP6 Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Weijie Wang ◽  
Yi Lin ◽  
Guanghui Zhang ◽  
Guofu Shi ◽  
Yongsheng Jiang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Progression ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Small Cell Lung ◽  
Antitumor Effects

Background. Accumulating articles have reported the pivotal regulatory roles of circular RNAs (circRNAs) in non-small-cell lung cancer (NSCLC) tumorigenesis. Here, our purpose was to explore the role of circ_0002346 in NSCLC progression and its associated mechanism. Methods. Cell proliferation ability was assessed by a 5-ethynyl-2 ′ -deoxyuridine (EDU) assay and a colony formation assay. Transwell assays were conducted to analyze cell migration and invasion abilities. Cell apoptosis was analyzed by flow cytometry and by using a caspase3 activity assay kit. The glycolysis of NSCLC cells was analyzed using a fluorescence-based glucose/lactate assay kit. A dual-luciferase reporter assay and an RNA pull-down assay were performed to verify the binding relationship between microRNA-582-3p (miR-582-3p) and circ_0002346 or syntaxin-binding protein 6 (STXBP6). Results. circ_0002346 level was prominently downregulated in NSCLC tissues and cell lines. circ_0002346 overexpression significantly suppressed the proliferation, migration, invasion, and glycolysis and triggered the apoptosis of NSCLC cells. circ_0002346 directly interacted with miR-582-3p, and circ_0002346 overexpression-mediated antitumor effects in NSCLC cells were partly reversed by miR-582-3p overexpression. miR-582-3p directly interacted with the 3 ′ untranslated region (3 ′ UTR) of STXBP6, and STXBP6 silencing partly counteracted circ_0002346 overexpression-mediated antitumor influences in NSCLC cells. circ_0002346 can upregulate the expression of STXBP6 by acting as a miR-582-3p sponge in NSCLC cells. circ_0002346 overexpression suppressed xenograft tumor growth in vivo. Conclusion. circ_0002346 overexpression suppressed the malignant properties of NSCLC cells by binding to miR-582-3p to induce the expression of STXBP6.

scholarly journals Diallyl Disulfide Attenuates Ionizing Radiation-Induced Migration and Invasion by Suppressing Nrf2 Signaling in Non–small-Cell Lung Cancer

Dose-Response ◽  
2021 ◽  
Vol 19 (3) ◽  
pp. 155932582110331
Author(s):  
Shuai Xu ◽  
Hefa Huang ◽  
Deping Tang ◽  
Mengjie Xing ◽  
Qiuyue Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Ionizing Radiation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Migration And Invasion ◽  
Diallyl Disulfide ◽  
Small Cell Lung ◽  
Antitumor Effects

Non–small-cell lung cancer (NSCLC) is the leading cause of cancer-associated deaths. Radiotherapy remains the primary treatment method for NSCLC. Despite great advances in radiotherapy techniques and modalities, recurrence and resistance still limit therapeutic success, even low-dose ionizing radiation (IR) can induce the migration and invasion. Diallyl disulfide (DADS), a bioactive component extracted from garlic, exhibits a wide spectrum of biological activities including antitumor effects. However, the effect of DADS on IR-induced migration and invasion remains unclear. The present study reported that IR significantly promoted the migration and invasion of A549 cells. Pretreatment with 40 μM DADS enhanced the radiosensitivity of A549 cells and attenuated IR-induced migration and invasion. In addition, 40 μM DADS inhibited migration-related protein matrix metalloproteinase-2 and 9 (MMP-2/9) expression and suppressed IR-aggravated EMT by the upregulation of the epithelial marker, E-cadherin, and downregulation of the mesenchymal marker, N-cadherin, in A549 cells. Furthermore, DADS was found to inhibit the activation of Nrf2 signaling. Based on our previous results that knockdown of Nrf2 by siRNA suppressed IR-induced migration and invasion in A549 cells, we speculated that DADS attenuated IR-induced migration and invasion by suppressing the activation of Nrf2 signaling in A549 cells.

The Key microRNAs Regulated the Development of Non-small Cell Lung Cancer by Targeting TGF-β-induced epithelial–mesenchymal Transition

2019 ◽  
Vol 22 (4) ◽  
pp. 238-244 ◽  
Author(s):  
Gang Chen ◽  
Bo Ye
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Nsclc Cell ◽  
Normal Lung ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
Mesenchymal Transition

Purpose: Epithelial-to-Mesenchymal Transition (EMT) was reported to play a key role in the development of Non-Small Cell Lung Cancer (NSCLC). The process of EMT is regulated by the changes of miRNAs expression. However, it is still unknown which miRNA changed the most in the process of canceration and whether these changes played a role in tumor development. Methods: A total of 36 SCLC patients treated in our hospital between 11th, 2015 and 10th, 2017 were enrolled. The samples of cancer tissues and paracancer tissues of patients were collected and analyzed. Then, the miRNAs in normal lung cells and NSCLC cells were also analyzed. In the presence of TGF-β, we transfected the miRNA mimics or inhibitor into NSCLC cells to investigate the role of the significantly altered miRNAs in cell migration and invasion and in the process of EMT. Results: MiR-330-3p was significantly up-regulated in NSCLC cell lines and tissues and miRNA- 205 was significantly down-regulated in NSCLC cell lines and NSCLC tissues. Transfected miRNA-205 mimics or miRMA-330-3p inhibitor inhibited the migration and invasion of NCIH1975 cell and restrained TGF-β-induced EMT in NSCLC cells. Conclusion: miRNA-330-3p and miRNA-205 changed the most in the process of canceration in NSCLC. Furthermore, miR-330-3p promoted cell invasion and metastasis in NSCLC probably by promoting EMT and miR-205 could restrain NSCLC likely by suppressing EMT.

Comparative Proteomics and Bioinformatics Analysis of Tissue from Non-Small Cell Lung Cancer Patients

2017 ◽  
Vol 14 (1) ◽  
pp. 58-77
Author(s):  
Sevgi Gezici ◽  
Mehmet Ozaslan ◽  
Gurler Akpinar ◽  
Murat Kasap ◽  
Maruf Sanli ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Patients ◽  
Cell Lung Cancer ◽  
Bioinformatics Analysis ◽  
Comparative Proteomics ◽  
Small Cell ◽  
Small Cell Lung ◽  
Lung Cancer Patients

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 Predicting ROR1/BCL2 combination targeted therapy of small cell carcinoma of the lung

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Walter Z. Wang ◽  
Konstantin Shilo ◽  
Joseph M. Amann ◽  
Alyssa Shulman ◽  
Mohammad Hojjat-Farsangi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Targeted Therapy ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Therapeutic Target ◽  
Small Cell ◽  
Orphan Receptor ◽  
Small Cell Lung ◽  
Sclc Patient

AbstractSmall cell lung cancer (SCLC) remains a deadly form of cancer, with a 5-year survival rate of less than 10 percent, necessitating novel therapies. Receptor tyrosine kinase-like orphan receptor 1 (ROR1) is an oncofetal protein that is emerging as a therapeutic target and is co-expressed with BCL2 in multiple tumor types due to microRNA coregulation. We hypothesize that ROR1-targeted therapy is effective in small cell lung cancer and synergizes with therapeutic BCL2 inhibition. Tissue microarrays (TMAs) and formalin-fixed paraffin-embedded (FFPE) SCLC patient samples were utilized to determine the prevalence of ROR1 and BCL2 expression in SCLC. Eight SCLC-derived cell lines were used to determine the antitumor activity of a small molecule ROR1 inhibitor (KAN0441571C) alone and in combination with the BCL2 inhibitor venetoclax. The Chou-Talalay method was utilized to determine synergy with the drug combination. ROR1 and BCL2 protein expression was identified in 93% (52/56) and 86% (48/56) of SCLC patient samples, respectively. Similarly, ROR1 and BCL2 were shown by qRT-PCR to have elevated expression in 79% (22/28) and 100% (28/28) of SCLC patient samples, respectively. KAN0441571C displayed efficacy in 8 SCLC cell lines, with an IC50 of 500 nM or less. Synergy as defined by a combination index of <1 via the Chou-Talalay method between KAN0441571C and venetoclax was demonstrated in 8 SCLC cell lines. We have shown that ROR1 inhibition is synergistic with BCL2 inhibition in SCLC models and shows promise as a novel therapeutic target in SCLC.

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