Is this just a strange coincidence (like the other anagram, Moronic), or is it another piece in this attempt to destroy all of humanity ?
Only time will tell.
Oncomir, a tumor-associated microRNA. Is it just an odd coincidence ?
It has been almost three years since I wrote this article.
Once again, it seems to have hit the mark.
Unfortunately, it certainly wasn’t hard to predict.
December 1, 2021
A nucleotide is the basic building block of nucleic acids. RNA and DNA are polymers made up of long chains of nucleotides. A nucleotide consists of a sugar molecule (ribose in RNA or deoxyribose in DNA) to which a phosphate group and a nitrogenous base are attached. The bases used in DNA are: adenine (A), cytosine (C), guanine (G), and thymine (T). In RNA, thymine is replaced with uracil (U).
An oncomir is a microRNA that is associated with a tumor.
MicroRNAs are small RNA molecules approximately 22 nucleotides in length.
Essentially, microRNAs target specific messenger RNAs (mRNAs) to prevent the translation of a specific protein.
Dysregulation of certain microRNAs (oncomirs) has been associated with specific tumorigenic events (oncogenes).
Some are oncogenes in the sense that gene overexpression leads to tumor growth.
Others are oncosuppressors, genes that encode products that inhibit cell cycle progression and protect cells from the accumulation of potentially cancerous mutations.
Some tumors may be “oncomir-dependent”, i.e. a constant level of oncomir is required to keep the tumor alive.
This is demonstrated by the inactivation of the oncomir miR-21.
Mice expressing miR-21 developed tumors of the pre-B malignant lymphoid type.
Studies have been conducted to evaluate the efficacy of microRNAs as potential markers for cancer diagnosis.
MicroRNAs have shown promise in this area due to their stability and ability to distinguish healthy cells from cancerous cells.
A recent study investigated the use of miRNAs as biomarkers in pancreatic ductal adenocarcinoma, a type of pancreatic cancer.
The study analyzed RNA from biopsied pancreatic cysts to identify changes in miRNA expression.
Extracellular microRNAs (exRNAs) may also be useful for the clinical diagnosis of cancer.
For example, in a study of patients with a type of lymphoma called diffuse large B-cell lymphoma (DLBCL), serum levels of three microRNAs, miR-21, miR-155 and miR-210, were higher in cancer patients than in healthy individuals.
The oncomiR-1 miRNA cluster is one of the best characterized mammalian oncogenic miRNA clusters.
The oncomiR-1 gene, also known as mir-17-92, encodes a single mRNA transcript that folds into six stem loops.
Several cancer-associated oncogenes are generated from these stem loops, including miRNAs 17, 18, 19a, 20, 19b and 92.
The miRNAs of the OncomiR-1 line have been shown to inhibit cell death, so that increased expression of oncomir-1 leads to tumor formation.
OncomiR-1 products inhibit the expression of the transcription factor E2F1, which can affect apoptosis through the ARF-p53 pathway.
It is estimated that there are several hundred target mRNAs for each miRNA, suggesting the presence of many additional potential targets for the OncomiR-1 line.
OncomiR resources and databases
Currently, three online databases are available for the collection and annotation of oncogenic and tumor miRNAs :
OncoMir Cancer Database : online database providing access to microRNA expression data based on microRNA sequencing miRCancer: microRNA cancer association database Oncomir: a collection of microRNA expression databases
MicroRNA-17, or miR-17, is a member of the OncomiR-1 family and was one of the first microRNAs identified as an oncogene.
miR-17 has been confirmed as a target of the cell cycle transcription factor E2F1, a protein that promotes not only cell growth but also cell death.
MicroRNA-19, or miR-19, is a member of the OncomiR-1 family and consists of three sub-classifications in both humans and mice: mir-19a, mir-19b1 and mir-19b2.
miR-19 has been shown to downregulate phosphatase and tensin homolog (PTEN), effectively increasing the activity of the PI3K-Akt signaling pathway that promotes cell survival.
MicroRNA-21, or miR-21, is a specific Oncomir that replicates rapidly in human cancers.
Increased microRNA-21 has been found in a wide range of cancers, including glioblastoma, breast cancer, colorectal cancer, lung cancer, pancreatic cancer, skin cancer, liver cancer, gastric cancer, cervical cancer, thyroid cancer, and various lymphatic and hematopoietic cancers.
MicroRNA-155, or miR-155, is an oncomir that is frequently overexpressed in human cancers.
In breast cancer, it has been identified as a target of the gene encoding for a protein called suppressor of cytokine signaling 1 (SOCS1).
Overexpression of this microRNA in breast epithelial cells leads to downregulation of a tumor suppressor gene.
Cell growth is increased.
A strong association has been found between miR-569 and the chromosomal locus 3q26.2, which is amplified in some breast cancers.
Altered expression of the miR-569 gene has been shown to affect the growth and proliferation of breast epithelial cells.
Ectopic expression of miR-569 has been shown to lead to cancer cell proliferation and metastasis.
This is due to the inhibition of TP53INP1, a tumor suppressor gene, by miR-569.
Compared to normal tissue and less malignant tumors, lower levels of TP53INP1 are found in more invasive tumors, presumably due in part to the role of miR-569.
Let-7 is the first anti-cancer cytokine identified that functions as a post-transcriptional gatekeeper of certain genes that control cell growth.
In lung cancer, for example, some oncogenes are down-regulated by Let-7, allowing normal cell progression to be maintained.
Tumor formation has been observed when miR-143 and miR-145 are downregulated, particularly in colon and gastric cancer cells.
When expressed in colon cancer cells, miR-143 and miR-145 are able to slow growth at the translational level by interfering with MAPK7, an enzyme responsible for cell growth.
In therapeutics, chemical devitalization (i.e. artificial modification) of miR-143 and miR-145 may prove to be a more effective option than their natural counterparts.
In particular, the modified miRNAs may be more resistant to nucleases that would otherwise degrade them.
