Role of 4-O Galloylchlorogenic Acid in Lung Cancer- An Insilico Approach

2017 ◽  
Vol 9 (5) ◽  
Author(s):  
Jaynthy C. ◽  
N. Premjanu ◽  
Abhinav Srivastava
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
In Silico ◽  
Computational Study ◽  
Regulation Mechanism ◽  
Down Regulation ◽  
Fruit Extract ◽  
In Vitro Techniques ◽  
Discovery Studio

Cancer is a major disease with millions of patients diagnosed each year with high mortality around the world. Various studies are still going on to study the further mechanisms and pathways of the cancer cell proliferation. Fucosylation is one of the most important oligosaccharide modifications involved in cancer and inflammation. In cancer development increased core fucosylation by FUT8 play an important role in cell proliferation. Down regulation of FUT8 expression may help cure lung cancer. Therefore the computational study based on the down regulation mechanism of FUT8 was mechanised. Sapota fruit extract, containing 4-Ogalloylchlorogenic acid was used as the inhibitor against FUT-8 as target and docking was performed using in-silico tool, Accelrys Discovery Studio. There were several conformations of the docked result, and conformation 1 showed 80% dock score between the ligand and the target. Further the amino acids of the inhibitor involved in docking were studied using another tool, Ligplot. Thus, in-silico analysis based on drug designing parameters shows that the fruit extract can be studied further using in-vitro techniques to know its pharmacokinetics.

scholarly journals Bauhinia acuminata L. attenuates lung cancer cell proliferation: in vitro, in vivo and in silico approaches

2021 ◽  
pp. 100173
Author(s):  
Divya Sebastian ◽  
K. Gowrishankar ◽  
S. Ignacimuthu ◽  
A.J. Renilda Sophy ◽  
R. Vidhya ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
In Silico ◽  
Cancer Cell Proliferation ◽  
Lung Cancer Cell ◽  
Proliferation In Vitro

scholarly journals Integrated bioinformatic analysis of miR-654-5p target genes and experimental validation of functional analyses

2020 ◽  
Author(s):  
Chuanyang Liu ◽  
Lu Min ◽  
Jingyu Kuang ◽  
Chu-shu Zhu ◽  
Jia-xin Ma ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
In Silico ◽  
Experimental Validation ◽  
Target Genes ◽  
Main Function ◽  
Hub Genes ◽  
Pan Cancer

AbstractBackgroundLung cancer is one of the most malignant types of cancer worldwide. Recently, the pivotal role of miRNAs in carcinogenesis and tumor metastasis have been reported for their direct regulation of specific target genes. However, the precise roles of miR-654-5p in lung adenocarcinoma have been poorly investigated. In this study, we designed a series of closed-loop integrated bioinformatic analyses and in vitro experimental validation to explore the main function and regulation pattern of miR-654-5p, and elucidate its roles in lung adenocarcinoma metastasis and prognosis both in silico and in vitro.MethodData from The Cancer Genome Atlas (TCGA) were used to analyze the pan-cancer prognostic value of miR-654-5p. miRanda, TargetScan, RNA22 and miRWalks were utilized to screen the targets of miR-654-5p. Metascape and miRWalks were used to perform gene ontology analyses and multiple enrichment analyses. STRING database and Cytoscape were used to construct protein-protein network and identify hub genes. GEPIA 2.0 were used to perform pan-cancer expression and survival analyses of hub genes. The regulation between miRNAs and predicted genes were verified by qPCR, western blotting and dual-luciferase system. In addition, EMT hallmarks detection, cell proliferation assay and wound healing assay were used to demonstrate the predicted functions of miR-654-5p experimentally.ResultsWe identified 275 potential targets of miR-654-5p and validated the direct regulatory effects of miR-654-5p on RNF8 in vitro as a proof of concept. Furthermore, we revealed the pivotal functions and disease association of miR-654-5p and experimentally validated the tumor suppressor roles of miR-645-5p that inhibited lung cancer cell epithelial-mesenchymal transition process, cell proliferation, and migration capacity. Among these 275 targets, 11 highly interconnected hub genes in lung adenocarcinoma were selected and studied through pan-cancer expression and pan-cancer survival analysis, in order to assess these targets’ clinical value.Conclusionsour research not only identified 275 hub target genes of miR-654-5p in silico and performed experimental validation but also revealed the tumor-suppressive roles of miR-654-5p in lung adenocarcinoma metastasis in vitro for the first time.

scholarly journals Aberrantly high activation of a FoxM1–STMN1 axis contributes to progression and tumorigenesis in FoxM1-driven cancers

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Jun Liu ◽  
Jipeng Li ◽  
Ke Wang ◽  
Haiming Liu ◽  
Jianyong Sun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Poor Prognosis ◽  
Soft Agar ◽  
Transcriptional Level ◽  
Regulation Mechanism ◽  
Strong Positive Correlation ◽  
Cell Viability Assay ◽  
High Level

AbstractFork-head box protein M1 (FoxM1) is a transcriptional factor which plays critical roles in cancer development and progression. However, the general regulatory mechanism of FoxM1 is still limited. STMN1 is a microtubule-binding protein which can inhibit the assembly of microtubule dimer or promote depolymerization of microtubules. It was reported as a major responsive factor of paclitaxel resistance for clinical chemotherapy of tumor patients. But the function of abnormally high level of STMN1 and its regulation mechanism in cancer cells remain unclear. In this study, we used public database and tissue microarrays to analyze the expression pattern of FoxM1 and STMN1 and found a strong positive correlation between FoxM1 and STMN1 in multiple types of cancer. Lentivirus-mediated FoxM1/STMN1-knockdown cell lines were established to study the function of FoxM1/STMN1 by performing cell viability assay, plate clone formation assay, soft agar assay in vitro and xenograft mouse model in vivo. Our results showed that FoxM1 promotes cell proliferation by upregulating STMN1. Further ChIP assay showed that FoxM1 upregulates STMN1 in a transcriptional level. Prognostic analysis showed that a high level of FoxM1 and STMN1 is related to poor prognosis in solid tumors. Moreover, a high co-expression of FoxM1 and STMN1 has a more significant correlation with poor prognosis. Our findings suggest that a general FoxM1-STMN1 axis contributes to cell proliferation and tumorigenesis in hepatocellular carcinoma, gastric cancer and colorectal cancer. The combination of FoxM1 and STMN1 can be a more precise biomarker for prognostic prediction.

Knockdown CYP2S1 inhibits lung cancer cells proliferation and migration

2021 ◽  
pp. 1-9
Author(s):  
Huan Guo ◽  
Baozhen Zeng ◽  
Liqiong Wang ◽  
Chunlei Ge ◽  
Xianglin Zuo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Lung Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

BACKGROUND: The incidence of lung cancer in Yunnan area ranks firstly in the world and underlying molecular mechanisms of lung cancer in Yunnan region are still unclear. We screened a novel potential oncogene CYP2S1 used mRNA microassay and bioinformation database. The function of CYP2S1 in lung cancer has not been reported. OBJECTIVE: To investigate the functions of CYP2S1 in lung cancer. METHODS: Immunohistochemistry and Real-time PCR were used to verify the expression of CYP2S1. Colony formation and Transwell assays were used to determine cell proliferation, invasion and migration. Xenograft assays were used to detected cell growth in vivo. RESULTS: CYP2S1 is significantly up-regulated in lung cancer tissues and cells. Knockdown CYP2S1 in lung cancer cells resulted in decrease cell proliferation, invasion and migration in vitro. Animal experiments showed downregulation of CYP2S1 inhibited lung cancer cell growth in vivo. GSEA analysis suggested that CYP2S1 played functions by regulating E2F targets and G2M checkpoint pathway which involved in cell cycle. Kaplan-Meier analysis indicated that patients with high CYP2S1 had markedly shorter event overall survival (OS) time. CONCLUSIONS: Our data demonstrate that CYP2S1 exerts tumor suppressor function in lung cancer. The high expression of CYP2S1 is an unfavorable prognostic marker for patient survival.

scholarly journals Nicotine promotes the development of non-small cell lung cancer through activating LINC00460 and PI3K/Akt signaling

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Hongying Zhao ◽  
Yu Wang ◽  
Xiubao Ren
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Akt Signaling ◽  
Small Cell ◽  
Nsclc Cell ◽  
Expression Level ◽  
In Vitro Experiments ◽  
Small Cell Lung

Abstract Objective: Nicotine, the main ingredient in tobacco, is identified to facilitate tumorigenesis and accelerate metastasis in tumor. Studies in recent years have reported that long intergenic non-protein coding RNA 460 (LINC00460) is strongly associated with lung cancer poor prognosis and nicotine dependence. Nonetheless, it is unclear whether nicotine promotes the development of lung cancer through activation of LINC00460. Methods: We determined that LINC00460 expression in lung cancer tissues and the prognosis in patients with non-small cell lung carcinoma (NSCLC) using Gene Expression Profiling Interactive Analysis (GEPIA) website and The Cancer Genome Atlas (TCGA) database. Through in vitro experiments, we studied the effects of nicotine on LINC00460 in NSCLC cells lines using Cell Counting Kit-8 (CCK-8), transwell test, flow cytometry, quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot assays. Results: We identified the significant up-regulated expression level of LINC00460 in NSCLC tissues and cell lines, especially, the negative correlation of LINC00460 expression level with overall survival (OS). In in vitro experiments, LINC00460 was overexpressed in NSCLC cell lines under nicotine stimulation. Nicotine could relieve the effect of LINC00460 knockdown on NSCLC cell proliferation, migration and apoptosis. The same influence was observed on PI3K/Akt signaling pathway. Conclusions: In summary, this is the first time to examine the potential roles of LINC00460 in lung cancer cell proliferation, migration and apoptosis induced by nicotine. This may help to develop novel therapeutic strategies for the prevention and treatment of metastatic tumors from cigarette smoke-caused lung cancer by blocking the nicotine-activated LINC00460 pathway.

In silico identification and in vitro validation of nogalamycin N ‐oxide (NSC116555) as a potent anticancer compound against non–small‐cell lung cancer cells

2018 ◽  
Vol 120 (3) ◽  
pp. 3353-3361 ◽  
Author(s):  
Phongphat Obounchoey ◽  
Lueacha Tabtimmai ◽  
Praphasri Suphakun ◽  
Kannika Thongkhao ◽  
Chatchakorn Eurtivong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
In Silico ◽  
Small Cell ◽  
Small Cell Lung ◽  
In Silico Identification ◽  
Anticancer Compound

scholarly journals Kaempferol-Mediated Sensitization Enhances Chemotherapeutic Efficacy of Sorafenib Against Hepatocellular Carcinoma: An In Silico and In Vitro Approach

2020 ◽  
Vol 10 (3) ◽  
pp. 472-476
Author(s):  
Bhagyalakshmi Nair ◽  
Ruby John Anto ◽  
Sabitha M ◽  
Lekshmi R. Nath
Keyword(s):  
Hepatocellular Carcinoma ◽  
Multidrug Resistance ◽  
Liver Cancer ◽  
In Silico ◽  
Culture Media ◽  
Positive Control ◽  
Advanced Hepatocellular Carcinoma ◽  
Discovery Studio ◽  
Toxic Concentrations

Purpose : Sorafenib is the sole FDA approved drug conventionally used for the treatment of advanced hepatocellular carcinoma (HCC). Despite of the beneficial use of sorafenib in the treatment of HCC, multidrug resistance still remains a challenge. HCC is inherently known as chemotherapy resistant tumor due to P-glycoprotein (P-gp)-mediated multidrug resistance. Methods: We studied the interaction energy of kaempferol with human multidrug resistance protein-1 (RCSB PDB ID: 2CBZ) using in silico method with the help of BIOVIA Discovery Studio. HepG2 and N1S1 liver cancer cell lines were treated in suitable cell culture media to evaluate the efficacy of kaempferol in chemo-sensitizing liver cancer cells towards the effect of sorafenib. Cell viability study was performed by MTT assay. Results: In silico analysis of kaempferol showed best docking score of 23.14 with Human Multi Drug Resistant Protein-1 (RCSB PDB ID: 2CBZ) compared with positive control verapamil. In in-vitro condition, combination of sub-toxic concentrations of both kaempferol and sorafenib produced 50% cytotoxicity with concentration of 2.5 µM each which indicates that kaempferol has the ability to reverse the MDR by decreasing the over-expression of P-gp. Conclusion: Kaempferol is able to sensitize the HepG2 and N1S1 against the sub-toxic concentration of sorafenib. Hence, we consider that the efficacy of sorafenib chemotherapy can be enhanced by the significant approach of combining the sub-toxic concentrations of sorafenib with kaempferol. Thus, kaempferol can be used as a better candidate molecule along with sorafenib for enhancing its efficacy, if validated through preclinical studies.

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