Редактирование: ENTPD7 (раздел)

==Publications==

{{medline-entry
|title=Inhibition of lung cancer cells and Ras/Raf/MEK/ERK signal transduction by ectonucleoside triphosphate phosphohydrolase-7 ([[ENTPD7]]).
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31443651
|abstract=The aim of this study was to investigate the effects and mechanisms of ectonucleoside triphosphate phosphohydrolase-7 ([[ENTPD7]]) on lung cancer cells. The expression characteristics of [[ENTPD7]] and its effect on the survival of lung cancer patients were analyzed by referring to The Cancer Genome Atlas (TCGA). Streptavidin-peroxidase (SP) staining was performed to detect the [[ENTPD7]] protein in tumor tissues and adjacent tissues. Plasmid transfection technology was also applied to silence [[ENTPD7]] gene. Crystal violet staining and flow cytometry were performed to determine cell proliferation and apoptosis. Tumor-bearing nude mice model was established to investigate the effect of sh-[[ENTPD7]] on tumors. The results showed that patients with low levels of [[ENTPD7]] had higher survival rates. [[ENTPD7]] was up-regulated in lung cancer tissues and cells. Down-regulation of the expression of [[ENTPD7]] inhibited proliferation but promoted apoptosis of lung cancer cell. Silencing [[ENTPD7]] also inhibited the expression levels of Ras and Raf proteins and the phosphorylation of mitogen-activated protein kinase (MEK) and extracellular signal-regulated kinase (ERK). Tumor-bearing nude mice experiments showed that silencing [[ENTPD7]] had an inhibitory effect on lung cancer cells. [[ENTPD7]] was overexpressed in lung cancer cells. Down-regulating [[ENTPD7]] could inhibit lung cancer cell proliferation and promote apoptosis via inhibiting the Ras/Raf/MEK/ERK pathway.
|mesh-terms=* Adult
* Aged
* Animals
* Apoptosis
* Apyrase
* Biomarkers
* Cell Line, Tumor
* Cell Proliferation
* Cells, Cultured
* Female
* Gene Expression Regulation, Neoplastic
* Gene Silencing
* Humans
* Lung Neoplasms
* MAP Kinase Signaling System
* Male
* Mice
* Mice, Inbred BALB C
* Mice, Nude
* Middle Aged
* Mitogen-Activated Protein Kinases
* Plasmids
* Signal Transduction
* Survival Analysis
* raf Kinases
* ras Proteins
|keywords=* Ectonucleoside triphosphate phosphohydrolase-7
* Lung cancer
* Proliferation
* Senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6708200
}}
{{medline-entry
|title=SWI/SNF regulates a transcriptional program that induces senescence to prevent liver cancer.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27737960
|abstract=Oncogene-induced senescence (OIS) is a potent tumor suppressor mechanism. To identify senescence regulators relevant to cancer, we screened an shRNA library targeting genes deleted in hepatocellular carcinoma (HCC). Here, we describe how knockdown of the SWI/SNF component [[ARID1B]] prevents OIS and cooperates with RAS to induce liver tumors. [[ARID1B]] controls p16  and p21  transcription but also regulates DNA damage, oxidative stress, and p53 induction, suggesting that SWI/SNF uses additional mechanisms to regulate senescence. To systematically identify SWI/SNF targets regulating senescence, we carried out a focused shRNA screen. We discovered several new senescence regulators, including [[ENTPD7]], an enzyme that hydrolyses nucleotides. [[ENTPD7]] affects oxidative stress, DNA damage, and senescence. Importantly, expression of [[ENTPD7]] or inhibition of nucleotide synthesis in [[ARID1B]]-depleted cells results in re-establishment of senescence. Our results identify novel mechanisms by which epigenetic regulators can affect tumor progression and suggest that prosenescence therapies could be employed against SWI/SNF-mutated cancers.
|mesh-terms=* Animals
* Apyrase
* Carcinoma, Hepatocellular
* Cell Line
* Cell Line, Tumor
* Cellular Senescence
* DNA-Binding Proteins
* Epigenesis, Genetic
* Female
* Gene Expression Regulation, Neoplastic
* Humans
* Liver Neoplasms
* Male
* Mice
* Mice, Inbred C57BL
* Mutation
* RNA, Small Interfering
* Transcription Factors
|keywords=* ARID1B
* ENTPD7
* SWI/SNF
* cancer
* dNTP metabolism
* p53
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5088567
}}