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Cancer: Lung Cancer

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Total 1667 results found since Jan 2013.

Down-regulation of eIF5A-2 prevents epithelial-mesenchymal transition in non-small-cell lung cancer cells.
Conclusions: The expression of eIF5A-2 was up-regulated following EMT phenotype changes in A549 cells, which correlated with enhanced tumor invasion and metastatic capabilities. Furthermore, in the A549 cell line, the process of EMT phenotype change could be reversed by eIF5A-2 siRNA, with a consequent weakening of both invasive and metastatic capabilities. PMID: 23733422 [PubMed - in process]
Source: J Zhejiang Univ Sci ... - June 1, 2013 Category: Science Authors: Xu GD, Shi XB, Sun LB, Zhou QY, Zheng DW, Shi HS, Che YL, Wang ZS, Shao GF Tags: J Zhejiang Univ Sci B Source Type: research

Wilms' tumour suppressor gene 1 (WT1) is involved in the carcinogenesis of Lung cancer through interaction with PI3K/Akt pathway
Although studies have shown the oncogene WT1 is overexpressed in lung cancer, there is no data showing the implication of WT1 in lung cancer biology. In the present study, we first demonstrated that isotype C of WT1 was conservely overexpressed in 20 lung cancer patient specimens. Knockdown of WT1 by small interference RNA (siRNA) transfection resulted in a significant inhibition of cell proliferation, induction of cell cycle arrest at G1 phase, and the expression change of BCL-2 family genes in WT1+ A549 cells. Furthermore, we found that DDP treatment could decrease the WT1 mRNA expression level by 5% and 15% at a dose of...
Source: Cancer Cell International - November 14, 2013 Category: Cancer & Oncology Authors: Xi WangPing GaoFang LinMin LongYuanyuan WengYongri OuyangLi LiuJunxia WeiXi ChenTing HeHuizhong ZhangKe Dong Source Type: research

Wilms¿ tumour suppressor gene 1 (WT1) is involved in the carcinogenesis of Lung cancer through interaction with PI3K/Akt pathway
AbsractAlthough studies have shown the oncogene WT1 is overexpressed in lung cancer, there is no data showing the implication of WT1 in lung cancer biology. In the present study, we first demonstrated that isotype C of WT1 was conservely overexpressed in 20 lung cancer patient specimens. Knockdown of WT1 by small interference RNA (siRNA) transfection resulted in a significant inhibition of cell proliferation, induction of cell cycle arrest at G1 phase, and the expression change of BCL-2 family genes in WT1+ A549 cells. Furthermore, we found that DDP treatment could decrease the WT1 mRNA expression level by 5% and 15% at a ...
Source: Cancer Cell International - November 14, 2013 Category: Cancer & Oncology Authors: Xi WangPing GaoFang LinMin LongYuanyuan WengYongri OuyangLi LiuJunxia WeiXi ChenTing HeHuizhong ZhangKe Dong Source Type: research

EZH2 Silencing with RNA Interference Induces G2/M Arrest in Human Lung Cancer Cells In Vitro.
This study clearly demonstrates that modulation of EZH2 expression with siRNA affects the cell cycle and the expression levels of p53 and p21, thereby changing cyclin B1 and Cdc2 expression and inducing G2/M arrest. These results may explain the observed antitumor activity of EZH2 silencing. Such explorations of the molecular mechanism of EZH2 will help us develop novel approaches to the diagnosis, treatment, and prevention of nonsmall-cell lung cancer. PMID: 24745014 [PubMed - in process]
Source: Biomed Res - April 23, 2014 Category: Research Authors: Xia H, Zhang W, Li Y, Guo N, Yu C Tags: Biomed Res Int Source Type: research

MicroRNA-182 modulates chemosensitivity of human non-small cell lung cancer to cisplatin by targeting PDCD4
Background: Overexpression of microRNA-182 (miR-182) is found in various human cancers, including non-small cell lung cancer (NSCLC). Our aim is to investigate the association of miR-182 expression with the sensitivity of NSCLC to cisplatin. Methods: TaqMan RT-PCR or Western blot assay was performed to detect the expression of mature miR-182 and programmed cell death 4 (PDCD4) protein. miR-182 and (or) PDCD4 depleted cell lines were generated using miR-182 inhibitor and (or) siRNA. The viabilities of treated cells were analyzed using MTT assay. Results: The expression level of miR-182 in A549 cell line was significantly hi...
Source: Diagnostic Pathology - July 10, 2014 Category: Pathology Authors: Fang-ling NingFeng WangMian-li LiZe-shun YuYan-zhang HaoShao-shui Chen Source Type: research

Down-regulated βIII-tubulin Expression Can Reverse Paclitaxel Resistance in A549/Taxol Cells Lines
Background and objective Chemotherapy drug resistance is the primary causes of death in patients with pulmonary carcinoma which make tumor recurrence or metastasis. β-tubulin is the main cell targets of anti-microtubule drug. Increased expression of βIII-tubulin has been implicated in non-small cell lung cancer (NSCLC) cell lines. To explore the relationship among the expression level of βIII-tubulin and the sensitivity of A549/Taxolcell lines to Taxol and cell cycles and cell apoptosis by RNA interference-mediated inhibition of βIII-tubulin in A549/Taxol cells. Methods Three pairs of siRNA targetd βIII-tubulin were d...
Source: Chinese Journal of Lung Cancer - August 18, 2014 Category: Cancer & Oncology Source Type: research

Expression and clinical significance of Semaphorin4D in non-small cell lung cancer and its impact on malignant behaviors of A549 lung cancer cells
This study aimed to explore Semaphrin4D (Sema4D) expression and clinical significance in non-small cell lung cancer (NSCLC), and to define the roles and mechanisms of Sema4D in regulating the malignant behaviors of A549 cells by small interfering RNA (siRNA). Firstly, immunohistochemistry revealed that Sema4D was more frequently expressed in NSCLC than in lung benign lesion (P<0.05) and its overexprssion was associated with low differentiation (P<0.05), poor pTNM staging (P<0.05) and occurrence of lymph node (LN) metastasis (P<0.05). Endogenous Sema4D expression was suppressed by Sema4D siRNA in A549 cells over...
Source: Journal of Huazhong University of Science and Technology -- Medical Sciences -- - August 1, 2014 Category: Research Source Type: research

Abstract 854: Inhibition of PRMT5 results in radiosensitization in lung cancer cell lines
Conclusion: PRMT5 inhibition by siRNA or its specific inhibitors lead to radiosensitivity in A549 lung cancer cell line. This effect may be partially dependent on p53-dependent cell cycle arrest. Further work to inhibit PRMT5 in other lung cancer cell lines with different p53 activities will be investigated. Citation Format: Smitha Sharma, X Wu, P Smith, N Denko, C Li, H Lai, F Yan, K Shilo, A Chakravarti, S Sif, R Baiocchi, G Otterson, Meng Xu-Welliver. Inhibition of PRMT5 results in radiosensitization in lung cancer cell lines. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Sharma, S., Wu, X., Smith, P., Denko, N., Li, C., Lai, H., Yan, F., Shilo, K., Chakravarti, A., Sif, S., Baiocchi, R., Otterson, G., Xu-Welliver, M. Tags: Clinical Research (Excluding Clinical Trials) Source Type: research

Abstract 2671: Targeting the KRAS signaling naocluster protein CNKSR1 provides antitumor activity against mutant KRAS xenografts
KRAS, the predominant form of mutated RAS (mut-KRAS) is found in 25% of patient tumors across many cancer types and plays a critical role in driving tumor growth and resistance to therapy. Its effects are so powerful that it overrides the activity of many molecularly targeted signaling drugs being developed for cancer today such that they cannot be used in patients with mut-KRAS. We have identified genes that when inhibited block the growth of mut-KRAS cancer cells without affecting wild type-KRAS (wt-KRAS) cell growth using a global siRNA screen. A top hit was CNKSR1 (connector enhancer of kinase suppressor of Ras 1), a p...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Triana-Balzer, G., Indarte, M., Scott, M., Powis, G., Kirkpatrick, D. L. Tags: Experimental and Molecular Therapeutics Source Type: research

Radiation-induced VEGF-C expression and endothelial cell proliferation in lung cancer
Conclusions Radiation-induced activation of the PI3K/Akt/mTOR signaling pathway increases VEGF-C expression in lung cancer cells, thereby promoting endothelial cell proliferation.
Source: Strahlentherapie und Onkologie - November 1, 2014 Category: Cancer & Oncology Source Type: research

Abstract 757: Activation of receptor-interacting serine/threonine protein kinase-2 (RIP2K) via EGFR-mediated CRAF transactivation induces the acquired resistance to Dabrafenib in BRAF V600E mutant non-small cell lung cancer
Discussion: Taken together, these findings suggest that the acquired resistance to Dabrafenib in BRAF V600E mutant NSCLC is uniquely mediated by EGFR-RAS-RIPK2-ERK signaling, bypassing MEK1/2, which may necessitate therapeutic strategies different from those of melanoma.Citation Format: Kangwon Jang, Jinyoung Sohn, Sung-Moo Kim, Kyoung Jin Kim, Byoung Chul Cho. Activation of receptor-interacting serine/threonine protein kinase-2 (RIP2K) via EGFR-mediated CRAF transactivation induces the acquired resistance to Dabrafenib in BRAF V600E mutant non-small cell lung cancer. [abstract]. In: Proceedings of the 106th Annual Meeting...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Jang, K., Sohn, J., Kim, S.-M., Kim, K. J., Cho, B. C. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 3555: Akt kinase-interacting protein1 as a potential therapeutics target in CREB1 signaling in malignant pleural mesothelioma
Conclusions:Our data suggest that Aki1/CREB axis may regulate the survival signaling, and may therefore be a potent target for DMM patients.Citation Format: Tadaaki Yamada, Joseph M. Amann, Konstantin Shilo, Naoya Fujita, Seiji Yano, David P. Carbone. Akt kinase-interacting protein1 as a potential therapeutics target in CREB1 signaling in malignant pleural mesothelioma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3555. doi:10.1158/1538-7445.AM2015-3555
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Yamada, T., Amann, J. M., Shilo, K., Fujita, N., Yano, S., Carbone, D. P. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 4956: Hsp27 negatively affects Hippo tumor suppressor pathway to regulate cell survival in cancer
Conclusion: Hsp27 overexpression contributes to inactivation of Hippo pathway. Targeting Hsp27 leads to inactivation of YAP and TAZ onco-proteins affecting cancer cell survival.Impact: Our data further supports the significance of targeting Hsp27 as a treatment option in cancers, especially metastatic malignancies like CRPC.Citation Format: Sepideh Vahid, Daksh Thaper, Amina Zoubeidi. Hsp27 negatively affects Hippo tumor suppressor pathway to regulate cell survival in cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelph...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Vahid, S., Thaper, D., Zoubeidi, A. Tags: Molecular and Cellular Biology Source Type: research

Suppression of nucleosome-binding protein 1 by miR-326 impedes cell proliferation and invasion in non-small cell lung cancer cells.
Authors: Li D, Du X, Liu A, Li P Abstract Emerging studies have proposed microRNAs (miRNAs) as novel therapeutic tools for cancer therapy. Nucleosome-binding protein 1 (NSBP1) has been suggested as an oncogene in various types of human cancers. The present study aimed to identify a novel miRNA that could directly target and negatively modulate NSBP1 expression. We found that NSBP1 was highly expressed in non‑small cell lung cancer (NSCLC) cells, and knockdown of NSBP1 by NSBP1 small interfering RNA (siRNA) significantly suppressed NSCLC cell proliferation and invasion. Bioinformatics analysis revealed that miRâ€...
Source: Oncology Reports - November 11, 2015 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

Phosphatidylethanolamine-binding protein 4 promotes lung cancer cells proliferation and invasion via PI3K/Akt/mTOR axis.
CONCLUSIONS: The overexpression of PEBP4 increases the phosphorylation levels of Akt and mTOR in lung cancer cells. The PI3K/Akt/mTOR signaling axis may be a key molecular pathway via which PEBP4 promotes the proliferation and invasion of non-small cell lung cancer (NSCLC) cells; also, it may serve as a potential therapeutic target. PMID: 26623104 [PubMed - as supplied by publisher]
Source: Journal of Thoracic Disease - December 4, 2015 Category: Respiratory Medicine Tags: J Thorac Dis Source Type: research