scholarly journals LncRNA HAND2-AS1 inhibits proliferation and promotes apoptosis of non-small cell lung cancer cells by inactivating PI3K/Akt pathway

2020 ◽  
Vol 40 (11) ◽  
Author(s):  
Ting Gao ◽  
Xiaoqiang Dai ◽  
Yindi Jiang ◽  
Xiaopeng He ◽  
Shuli Yuan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Small Cell ◽  
Akt Pathway ◽  
Healthy Controls ◽  
Small Cell Lung ◽  
Nsclc Patients ◽  
Related Proteins

Abstract Background: Non-small cell lung cancer (NSCLC) is a major subtype of lung cancer and is correlated with high incidence and mortality rate. Functionality of lncRNA HAND2-AS1 is only reported in endometrioid endometrial carcinoma and osteosarcoma. In our study, the role of HAND2-AS1 in NSCLC was investigated. Methods: We first detected the expression of HAND2-AS1 in lung tissues and serum of both NSCLC patients and healthy controls by qRT-PCR. Correlation between HAND2-AS1 expression level and clinical data of NSCLC patients was analyzed by Chi-square test. NSCLC cells, and cell proliferation, cell apoptosis and expression of PI3K/Akt pathway-related proteins were detected by CCK-8 assay, cell apoptosis assay and Western blot, respectively. Results: HAND2-AS1 expression was significantly down-regulated in NSCLC. HAND2-AS1 and tumor size of NSCLC patients were closely associated. Serum HAND2-AS1 can be used to effectively distinguish osteosarcoma patients from healthy controls, and it can also be used to predict prognosis of osteosarcoma patients. HAND2-AS1 overexpression inhibited osteosarcoma cell proliferation, promoted cell apoptosis, and down-regulated phosphorylation of PI3K/Akt pathway-related proteins. PI3K/Akt pathway inhibitor showed no significant effects on HAND2-AS1 expression, but reduced its effects on cell proliferation and apoptosis. Conclusion: We conclude that HAND2-AS1 may suppress the proliferation of NSCLC cells by targeting PI3K/Akt pathway.

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 Rsf-1 Influences the Sensitivity of Non-Small Cell Lung Cancer to Paclitaxel by Regulating NF-κB Pathway and Its Downstream Proteins

2017 ◽  
Vol 44 (6) ◽  
pp. 2322-2336 ◽  
Author(s):  
Xitao Chen ◽  
Xiaodi Sun ◽  
Jingqian Guan ◽  
Junda Gai ◽  
Jilin Xing ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Flow Cytometry ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Protein Levels ◽  
H460 Cell ◽  
Xenograft Mice

Background/Aims: The therapeutic efficacy of paclitaxel is hampered by chemotherapeutic resistance in non-small cell lung cancer (NSCLC). Rsf-1 enhanced paclitaxel resistance via nuclear factor-κB (NF-κB) in ovarian cancer cells and nasopharyngeal carcinoma. This study assessed the function of Rsf-1 in the modulation of the sensitivity of NSCLC to paclitaxel via the NF-κB pathway. Methods: The mRNA and protein levels of the related genes were quantified by RT-PCR and Western blotting. Rsf-1 silencing was achieved with CRISPR/Cas9 gene editing. Cell cycle, migration and proliferation were tested with flow cytometry, transwell test and CCK8 test. Cell apoptosis was analyzed with flow cytometry and quantification of C-capase3. The parameters of the tumors were measured in H460 cell xenograft mice. Results: Rsf-1 was highly expressed in H460 and H1299 cells. Rsf-1 knockout caused cell arrest at the G1 phase, increased cell apoptosis, and decreased migration and cell proliferation. Rsf-1 knockout increased the inhibition of cell proliferation, the reduction in cell migration and the augment in cell apoptosis in paclitaxel treated H460 and H1299 cells. Rsf-1 knockout further enhanced the paclitaxel-mediated decrease in the volume and weight of the tumors in H460 cell xenograft mice. Helenalin and Rsf-1 knockout decreased the protein levels of p-P65, BcL2, CFLAR, and XIAP; hSNF2H knockout decreased the protein level of NF-κB p-P65 without altering Rsf-1 and p65 protein levels, while Rsf-1 and hSNF2H double knockout decreased the level of NF-κB p-P65, in H1299 and H460 cells. Conclusion: These results demonstrate that Rsf-1 influences the sensitivity of NSCLC to paclitaxel via regulation of the NF-κB pathway and its downstream genes.

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.

scholarly journals microRNA-195 Promotes Small Cell Lung Cancer Cell Apoptosis via Inhibiting Rap2C Protein-Dependent MAPK Signal Transduction

2020 ◽  
Vol 19 ◽  
pp. 153303382097754
Author(s):  
Jichun Tong ◽  
Jiawei Lu ◽  
Yajun Yin ◽  
Yeming Wang ◽  
Ke Zhang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Small Cell ◽  
Luciferase Reporter ◽  
Small Cell Lung ◽  
Cancer Tissues

This study aimed to explore the influences of microRNA-195 (miRNA-195)/Rap2C/MAPK in the proliferation and apoptosis of small cell lung cancer (SCLC) cells. QRT-PCR analysis were executed to evaluate miRNA-195 expression in lung cancer tissues and SCLC cells, and the western blot was implemented to monitor Rap2C protein level and uncovered whether the MAPK signaling pathway in lung cancer tissues and SCLC cells was activated. The CCK-8 experiment was performed to detect cell proliferation ability, and the flow cytometry was utilized to examine cell apoptosis level. Luciferase reporter gene system was executed to disclose the interaction between miRNA-195 and Rap2C. Subcutaneous implantation mouse models of SCLC cells were constructed to detect cell proliferation in vivo, and Kaplan-Meier method calculated patient survival. The expression of Rap2C was higher in lung cancer tissues and SCLC cells than in normal tissues and cells, while the expression of miRNA-195 was lower in lung cancer tissues and SCLC cells than in normal tissues and cells. miRNA-195 lower expression predicted showed reduced overall survival in lung cancer patients. Further loss of function and enhancement experiments revealed that miRNA-195 overexpression could significantly inhibit SCLC cell proliferation and promote cell apoptosis by upregulation of Bax and down-regulation of bcl-2; Luciferase reporter assay demonstrated that miRNA-195 could bind to Rap2C mRNA and inhibit its expression, Rap2C overexpression also related to the poorer prognosis of lung patients. Knockdown of Rap2C suppressed cell proliferation and expedited apoptosis. In addition, overexpression of Rap2C reversed miRNA-195-induced apoptosis and proliferation inhibition. Furthermore, miRNA195 prohibited the activation of MAPK signaling pathway by down-regulating Rap2C. These consequences indicated that miRNA-195 promotes the apoptosis and inhibits the proliferation of small cell lung cancer (SCLC) cells via inhibiting Rap2C protein-dependent MAPK signal transduction

scholarly journals MicroRNA‐4286 promotes cell proliferation, migration, and invasion via PTEN regulation of the PI3K/Akt pathway in non‐small cell lung cancer

2019 ◽  
Vol 8 (7) ◽  
pp. 3520-3531 ◽  
Author(s):  
Chunhua Ling ◽  
Xueting Wang ◽  
Jianjie Zhu ◽  
Haicheng Tang ◽  
Wenwen Du ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Small Cell Lung

scholarly journals Urinary exosomal long noncoding RNAs serve as biomarkers for early detection of non-small cell lung cancer

2021 ◽  
Author(s):  
Quan Lin ◽  
Danli Xie ◽  
Liangliang Pan ◽  
Yongliang Lou ◽  
Mengru Shi
Keyword(s):  
Lung Cancer ◽  
Tumor Cell ◽  
Small Cell Lung Cancer ◽  
Differential Expression ◽  
Kegg Pathway ◽  
Small Cell ◽  
Healthy Controls ◽  
Small Cell Lung ◽  
Pathway Analyses ◽  
Nsclc Patients

Objective: Increasing the efficiency of early diagnosis using noninvasive biomarkers is crucial for enhancing the survival rate of lung cancer patients. We explore the differential expression of non-small cell lung cancer (NSCLC) related lncRNAs in urinary exosomes in NSCLC patients and normal controls to diagnose lung cancer. Methods: A differential expression analysis between NSCLC patients and healthy controls was performed using microarrays. Gene ontology (GO) term and Kyoto encyclopedia of genes and genomes (KEGG) pathway analyses were used to predict potential functions of lncRNAs in NSCLC. QT-PCR was used to verify microarray results. Results: A total of 640 lncRNAs (70 up- and 570 down-regulated) were differentially expressed in NSCLC patients in comparison to healthy controls. Six lncRNAs were detected by QT-PCR. GO term and KEGG pathway analyses showed that differential lncRNAs were enriched in cellular component organization or biogenesis, as well as other biological processes and signaling pathways, such as the PI3K-AKT, FOXO, p53, and fatty acid biosynthesis. Conclusions: The differential lncRNAs in urinary exosomes are potential diagnostic biomarkers of NSCLC. The lncRNAs enriched in specific pathways may be associated with tumor cell proliferation, tumor cell apoptosis, and the cell cycle involved in the pathogenesis of NSCLC.

scholarly journals LncRNA SNHG10 is downregulated in non-small cell lung cancer and predicts poor survival

2020 ◽  
Author(s):  
Meng Liang ◽  
Linlin Wang ◽  
Chuanhua Cao ◽  
Shimao Song ◽  
feng wu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Gene Methylation ◽  
Poor Survival ◽  
Tumor Tissues ◽  
Nsclc Patients

Abstract Background: LncRNA SNHG10 has been reported to be an oncogenic lncRNA in liver cancer. However, its roles in non-small cell lung cancer (NSCLC) remains unknown. Methods: Tumor and paired non-tumor tissues were harvested from 62 NSCLC patients. RT-qPCR was used to detect the expression of SNHG10 and miR-21 in tissues. Overexpression experiments were used to evaluate the interaction between SNHG10 and miR-21 in NSCLC cells. CCK-8 assay was used to detect the cell proliferation. Results: We observed the expression of SNHG10 was down-regulated in non-small cell lung cancer (NSCLC) compared with that in non-tumor tissues. Moreover, we found that high expression levels of SNHG10 predicted favorable survival of NSCLC patients, and the expression of miR-21 were increased in NSCLC and inversely correlated with SNHG10 expression. In NSCLC cells, overexpression of SNHG10 resulted in increased miR-21 gene methylation and decreased miR-21 expression. Moreover, overexpression of SNHG10 attenuated the enhancing effect of miR-21 overexpression on cell proliferation. Conclusions: SNHG10 may involve in NSCLC cell proliferation by regulating the miR-21 gene methylation.

scholarly journals LncRNA SNHG10 is downregulated in non-small cell lung cancer and predicts poor survival

2020 ◽  
Author(s):  
Meng Liang ◽  
Linlin Wang ◽  
Chuanhua Cao ◽  
Shimao Song ◽  
Feng Wu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Expression Level ◽  
Small Cell Lung ◽  
Poor Survival ◽  
Tcga Dataset ◽  
Nsclc Patients

Abstract LncRNA SNHG10 has been characterized as an oncogenic lncRNA in liver cancer. By analyzing TCGA dataset we observed the downregulation of SNHG10 in non-small cell lung cancer (NSCLC), indicating its involvement in this disease. We then analyzed the role of SNHG10 in NSCLC.Tumor and paired non-tumor tissues were harvested from 62 NSCLC patients. Expression of SNHG10 and miR-21 in tissues was determined by RT-qPCR. Overexpression of SNHG10 or miR-21 in NSCLC cells was achieved and the interaction between them was analyzed. Cell proliferation was analyzed by CCK-8 assay.In this study we found that SNHG10 is downregulated in cancer tissues of NSCLC patients included in this study. High expression level of SNHG10 predicted favorable survival of NSCLC patients. Levels of miR-21 expression were increased in NSCLC and inversely correlated with SNHG10. In NSCLC cells, SNHG10 overexpression led to increased miR-21 gene methylation and decreased miR-21 expression level. In cell proliferation assay, SNHG10 overexpression attenuated the enhancing effect of miR-21 overexpression on cell proliferation. SNHG10 is downregulated in non-small cell lung cancer and predicts poor survival. It may downregulated miR-21 through methylation to suppress cancer cell proliferation.

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