scholarly journals Altered expression of phosphatase of regenerating liver gene family in non-small cell lung cancer

2011 ◽  
Author(s):  
Seung-Hyo Lee
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gene Family ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Regenerating Liver ◽  
Small Cell Lung ◽  
Altered Expression ◽  
Liver Gene ◽  
Phosphatase Of Regenerating Liver

Redox regulation of matrix metalloproteinase gene family in small cell lung cancer cells

2005 ◽  
Vol 39 (4) ◽  
pp. 373-381 ◽  
Author(s):  
Niramol Savaraj ◽  
Yingjie Wei ◽  
Hitoshi Unate ◽  
Pei-Man Liu ◽  
C.J. Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Matrix Metalloproteinase ◽  
Small Cell Lung Cancer ◽  
Gene Family ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Redox Regulation ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung

Altered expression of ACOX2 and other members of the peroxisome pathway in non-small cell lung cancer

Lung Cancer ◽  
2021 ◽  
Vol 156 ◽  
pp. S2
Author(s):  
Jane Sui ◽  
Petra Martin ◽  
Siobhan Nicholson ◽  
Sinead Cuffe ◽  
Stephen Finn ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Altered Expression

scholarly journals Curcumin-Induced Global Profiling of Transcriptomes in Small Cell Lung Cancer Cells

2021 ◽  
Vol 8 ◽  
Author(s):  
Fei Mo ◽  
Yinan Xiao ◽  
Hao Zeng ◽  
Dian Fan ◽  
Jinen Song ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Elevated Concentration ◽  
Small Cell Lung ◽  
Altered Expression ◽  
Apoptosis Rate ◽  
Anti Tumor Activity

BackgroundCurcumin, one of the promising candidates for supplementary therapy in cancer treatment, has been demonstrated by numerous preclinical and clinical evidence to be beneficial in treating various cancers. Apart from the critical role in a deluge of pathological processes, some mRNAs, in particular, microRNAs (miRNAs), are also involved in the anti-tumor activity. Therefore, our research focused on the possible effects of curcumin on small cell lung cancer (SCLC) cells and drew a comprehensive transcriptomes profile by high throughput sequencing to understand the molecular mechanism of curcumin as an anti-tumor agent.MethodsFirst, we calculated the apoptosis rate of H446 cells (a human SCLC cell line) cultured with curcumin. The high output sequencing uncovered the altered expression profile of genes and miRNAs. KEGG analysis selected the potential signal pathway associated with the antiproliferative property of curcumin. Finally, miRNAs significantly changed, as well as the regulatory roles of those miRNAs in cell apoptosis were determined.ResultThe apoptosis rate of H446 cells increased under the elevated concentration of curcumin treatment. And cell cycle-related genes downregulated in the curcumin-treated cells. Besides, miRNA-548ah-5p of a high level acted as a negative role in the anticarcinogenic activity of curcumin.ConclusionOur findings not only enriched the understanding of anti-tumor activity initiated by curcumin through figuring out the downregulated cell cycle-related pathways but also shed light on its novel therapeutic application.

scholarly journals PTEN Mutant Non-Small Cell Lung Cancer Require ATM to Suppress Pro-Apoptotic Signalling and Evade Radiotherapy

2021 ◽  
Author(s):  
Thomas Fischer ◽  
Oliver Hartmann ◽  
Michaela Reissland ◽  
Cristian Prieto-Garcia ◽  
Kevin Klann ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Damage ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Ex Vivo ◽  
Therapy Resistance ◽  
Genetic Alterations ◽  
Small Cell ◽  
Small Cell Lung ◽  
Altered Expression

Abstract BackgroundDespite advances in treatment of patients with non-small cell lung cancer, carriers of certain genetic alterations are prone to failure. One such factor frequently mutated, is the tumor suppressor PTEN. These tumors are supposed to be more resistant to radiation, chemo- and immunotherapy.ResultsWe demonstrate that loss of PTEN led to altered expression of transcriptional programs which directly regulate therapy resistance, resulting in establishment of radiation resistance. While PTEN-deficient tumor cells were not dependent on DNA‑PK for IR resistance nor activated ATR during IR, they showed a significant dependence for the DNA damage kinase ATM. Pharmacologic inhibition of ATM, via KU-60019 and AZD1390 at non-toxic doses, restored and even synergized with IR in PTEN-deficient human and murine NSCLC cells as well in a multicellular organotypic ex vivo tumor model.ConclusionPTEN tumors are addicted to ATM to detect and repair radiation induced DNA damage. This creates an exploitable bottleneck. At least in cellulo and ex vivo we show that low concentration of ATM inhibitor is able to synergise with IR to treat PTEN-deficient tumors in genetically well-defined IR resistant lung cancer models.

scholarly journals Multiple mechanisms for transcriptional regulation of the myc gene family in small-cell lung cancer.

1988 ◽  
Vol 8 (8) ◽  
pp. 3373-3381 ◽  
Author(s):  
G Krystal ◽  
M Birrer ◽  
J Way ◽  
M Nau ◽  
E Sausville ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gene Family ◽  
Gene Amplification ◽  
Cell Lung Cancer ◽  
Promoter Activity ◽  
Small Cell ◽  
Mrna Levels ◽  
Small Cell Lung ◽  
Myc Gene

The molecular mechanisms reported to regulate the expression of myc family genes are multiple and complex and include gene amplification, transcriptional activation, transcriptional attenuation, and mRNA stability. We have investigated which of these mechanisms are responsible for the extreme variation in myc gene family mRNA levels observed in human small-cell lung cancer cell lines. In addition to gene amplification, a block to nascent mRNA chain elongation, causing attenuation of transcription, is an important regulatory mechanism controlling the steady-state levels of c-myc and L-myc mRNA. The loss of transcriptional attenuation is correlated with overexpression of these two genes in cell lines which do not show gene amplification. Expression of c-myc mRNA appears to be dependent on promoter activity and attenuator function. In contrast, regulation of expression of the N-myc gene does not involve transcriptional attenuation; steady-state mRNA levels are correlated with promoter activity as well as gene amplification. We conclude that transcriptional regulation of each member of the myc gene family is accomplished by a different assortment of complex mechanisms, including gene copy number, promoter activation, and transcriptional attenuation. Interference at multiple points in this complex regulatory process appears to be an important mechanism by which small-cell lung cancer and other human tumors evade growth control.

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