«It wasn't known whether miR - 486
functioned as an oncogene or a tumor - suppressor gene in lung cancer,» says co-corresponding author Patrick Nana - Sinkam, MD, associate professor of medicine and a researcher with the OSUCCC — James Molecular Biology and Cancer Genetics Program.
«This function for BAI1 may have implications for cancer biology, since MDM2 can
function as an oncogene by degrading important tumor suppressors like p53.»
A microRNA — a small piece of RNA involved in regulating gene expression —
functions as an oncogene to drive the development of lung...
Not exact matches
«Once this novel tumor - homing agent binds to the EphA2 receptor, the
oncogene functions as a cancer - specific molecular Trojan horse for paclitaxel, carrying the drug inside the cancel cell, killing the cell, and thwarting metastasis,» said Maurizio Pellecchia, a professor of biomedical sciences at UCR's School of Medicine who led the research.
But mutated or dysfunctional Rb is associated with several major cancers and Cyclin D has long been described
as an
oncogene that promotes cancer because it was believed to inactivate the Rb tumor suppressor
function through a process called phosphorylation, which involves phosphate molecules being added to proteins, essentially turning them on or off.
The three Ras genes found in humans — H - Ras, K - Ras and N - Ras — were among the first to be linked to cancer development, and a new study led by VCU Massey Cancer Center researcher Paul Dent, Ph.D., has shown the recently approved breast cancer drug neratinib can block the
function of Ras
as well
as several other
oncogenes through an unexpected process.
In fact, KLF4 blocks senescence and apoptosis by repressing transcription of P53, whereas it can activate P21 - dependent cell - cycle arrest, and therefore, KLF4 can
function both
as a tumor suppressor and an
oncogene (33, 34).
p53 is therefore well - studied
as an
oncogene, or a gene that when not
functioning normally can contribute to a normal cell becoming cancerous.
Using a model where K - ras acts
as an
oncogene and initiates tumor formation, mice that were bred to not have Notch1
function showed an almost uniform distribution of about two cancerous lesions per mouse after 6 weeks, compared with approximately 14 tumors / mouse for those with Notch1
function still remaining.
«The genotoxicity of mainstream smoke carcinogens manifests
as mutations occurring in key cancer - related genes, i.e., proto -
oncogenes or tumor suppressor genes that control crucial cellular
functions, e.g., growth and survival, in lung tumors of active smokers.»