scholarly journals The role of Rac1 in the regulation of NF-kB activity, cell proliferation, and cell migration in non-small cell lung carcinoma

2012 ◽  
Vol 13 (8) ◽  
pp. 647-656 ◽  
Author(s):  
Adam Gastonguay ◽  
Tracy Berg ◽  
Andrew D. Hauser ◽  
Nathan Schuld ◽  
Ellen Lorimer ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma

Possible role of PPAR-γ and COX-2 receptor modulators in the treatment of Non-Small Cell lung carcinoma

2019 ◽  
Vol 124 ◽  
pp. 98-100 ◽  
Author(s):  
V.V.V. Ravi Kiran Ammu ◽  
Kusuma Kumari Garikapati ◽  
Praveen T. Krishnamurthy ◽  
Pavan Kumar Chintamaneni ◽  
Sai Kiran S.S. Pindiprolu
Keyword(s):  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Ppar Γ ◽  
Cox 2 ◽  
Receptor Modulators

scholarly journals CELF2 suppresses non-small cell lung carcinoma growth by inhibiting the PREX2-PTEN interaction

2019 ◽  
Vol 41 (3) ◽  
pp. 377-389 ◽  
Author(s):  
Yiu To Yeung ◽  
Suyu Fan ◽  
Bingbing Lu ◽  
Shuying Yin ◽  
Sen Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Phosphatase Activity ◽  
Lung Carcinoma ◽  
Rna Binding ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Low Grade ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Human Cancers

Abstract The phosphoinositide 3-kinase (PI3-K)/Akt signaling pathway is important in the regulation of cell proliferation through its production of phosphatidylinositol 3,4,5-triphosphate (PIP3). Activation of this pathway is frequently observed in human cancers, including non-small cell lung carcinoma. The PI3-K/Akt pathway is negatively regulated by the dual-specificity phosphatase and tensin homolog (PTEN) protein. PTEN acts as a direct antagonist of PI3-K by dephosphorylating PIP3. Studies have shown that PTEN phosphatase activity is inhibited by PREX2, a guanine nucleotide exchanger factor (GEF). Multiple studies revealed that CELF2, an RNA binding protein, cooperates synergistically with PTEN as a tumor suppressor in multiple cancers. However, the underlying mechanism as to how CELF2 enhances PTEN activity remains unclear. Here, we report that CELF2 interacts with PREX2 and reduces the association of PREX2 with PTEN. Consistent with this observation, PTEN phosphatase activity is upregulated with CELF2 overexpression. In addition, overexpression of CELF2 represses both Akt phosphorylation and cell proliferation only in the presence of PTEN. In an ex vivo study, CELF2 gene delivery could significantly inhibit patient-derived xenografts (PDX) tumor growth. To further investigate the clinical relevance of this finding, we analyzed 87 paired clinical lung adenocarcinoma samples and the results showed that CELF2 protein expression is downregulated in tumor tissues and associated with poor prognosis. The CELF2 gene is located on the chromosome 10p arm, a region frequently lost in human cancers, including breast invasive carcinoma, low-grade glioma and glioblastoma. Analysis of TCGA datasets showed that CELF2 expression is also associated with shorter patient survival time in all these cancers. Overall, our work suggests that CELF2 plays a novel role in PI3-K signaling by antagonizing the oncogenic effect of PREX2.

scholarly journals LncRNA HOXA-AS3 confers cisplatin resistance by interacting with HOXA3 in non-small-cell lung carcinoma cells

Oncogenesis ◽  
2019 ◽  
Vol 8 (11) ◽  
Author(s):  
Shuang Lin ◽  
Rui Zhang ◽  
Xiaoxia An ◽  
Zhoubin Li ◽  
Cheng Fang ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Lung Carcinoma ◽  
Cisplatin Resistance ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Cell Counting ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma

Abstract Many studies have indicated that the aberrant expression of long noncoding RNAs (lncRNAs) is responsible for drug resistance, which represents a substantial obstacle for cancer therapy. In the present study, we aimed to investigate the role of the lncRNA HOXA-AS3 in drug resistance and elucidate its underlying mechanisms in non-small-cell lung carcinoma (NSCLC) cells. The role of HOXA-AS3 in drug resistance was demonstrated by the cell counting kit-8 assay (CCK-8), ethynyldeoxyuridine (EDU) assay, and flow cytometry analysis. Tumor xenografts in nude mice were established to evaluate the antitumor effects of HOXA-AS3 knockdown in vivo. Western blotting and quantitative real-time PCR were used to evaluate protein and RNA expression. RNA pull-down assays, mass spectrometry, and RNA immunoprecipitation were performed to confirm the molecular mechanism of HOXA-AS3 in the cisplatin resistance of NSCLC cells. We found that HOXA-AS3 levels increased with cisplatin treatment and knockdown of HOXA-AS3 enhance the efficacy of cisplatin in vitro and in vivo. Mechanistic investigations showed that HOXA-AS3 conferred cisplatin resistance by down-regulating homeobox A3 (HOXA3) expression. Moreover, HOXA-AS3 was demonstrated to interact with both the mRNA and protein forms of HOXA3. In addition, HOXA3 knockdown increased cisplatin resistance and induced epithelial-mesenchymal transition (EMT). Taken together, our findings suggested that additional research into HOXA-AS3 might provide a better understanding of the mechanisms of drug resistance and promote the development of a novel and efficient strategy to treat NSCLC.

scholarly journals The role of the c-Jun N-terminal kinase 2-α-isoform in non-small cell lung carcinoma tumorigenesis

Oncogene ◽  
2010 ◽  
Vol 30 (2) ◽  
pp. 234-244 ◽  
Author(s):  
R T Nitta ◽  
C A Del Vecchio ◽  
A H Chu ◽  
S S Mitra ◽  
A K Godwin ◽  
...  
Keyword(s):  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma
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