New target for cancer-fighting potential - RUNX2.

Wen . . . In the course of development, many gene expressions become overactive, while others have lower expression.
these genetic changes help the tumor grow out of control, making it more aggressive and adaptable to changing circumstances, eventually causing the tumor to metastasize and spread to other parts of the body.
a new study published July 23 in the journal Cancer Cell, researchers from the Massachusetts Institute of Technology and Harvard University described a series of structural changes in chromosomals that control the evolution of cancer cells.
study of lung tumors in mice, researchers identified 11 chromosome states (also known as eigome states) as cancer cells became more aggressive.
researchers believe runX2, a key molecule found in the more aggressive tumor cell chroma state, is associated with advanced lung cancer in humans and could be used as a biomarker to predict patient prognostication.
Lindsay LaFave, lead author of the Cancer Cell study, said: "This work is the first example of a single-celled ethnometogenic data used to fully document tumor evolution regulation genes in cancer.
" egenetic control Although the cell's genome contains all of the cell's genetic material, the etogenome plays a key role in determining which of these genes will be expressed.
the genome of each cell has estensive genetic modifications, such as proteins and compounds attached to DNA that do not change the DNA sequence.
modification varies by cell type, affecting gene expression characteristics, as well as the differentiation of different kinds of cells, such as lung cells and neurons.
studies have suggested that egestic changes can affect the progression of cancer.
study, the team analyzed changes in the e general genome as lung tumors developed in mice.
study was a mouse model of lung adenocarcinoma, which is caused by two specific genetic mutations that can better summarize the development of human lung tumors. Using a new technique previously developed by Dr. Jason Buenrostro, one of the authors of the paper's communications, the
team analyzed the etogenetic changes that occur in tumor cells from an early stage to a more invasive stage, in addition to examining tumor cells transferred outside the lungs.
Based on where eigene genetic changes occur and the density of chromoses, this analysis revealed 11 different chromosic states in cancer cells (below), and that these 11 states of cells may exist in a single tumor, suggesting that cancer cells can follow different evolutionary pathways.
source: Cancer Cell researchers also determined the corresponding changes in the location of transcription factors and chromosome binding in each chromosome state.
when transcription factors bind to the gene's initiator region, the transcription of the gene's mRNA is initiated, essentially controlling the activity of the gene being bonded.
chromosogen modification to some extent enables the gene's initiators to bind to transcription factors.
changes in the chromosate structure of tumor cells, transcription factors tend to target genes that help cancer cells get rid of lung cell "identity" and reduce differentiation.
eventually most tumor cells will gain the ability to leave their original position and produce new tumors.
most of this process is controlled by the transcription factor RUNX2.
in more invasive cancer cells, RUNX2 promotes gene transcription of proteins secreted by cells.
these proteins help reshape the environment around the tumor, making it easier for cancer cells to escape (below).
: Cancer Cell researchers also found that these invasive prestasy tumor cells are very similar to metastatic tumor cells.
" suggests that when the tumor cells are in primary tumors before metastasis, they actually change their chromosic state, making them look like metastatic cells, and then migrate to the environment.
we believe that these tumor cells can metastasized and spread to remote locations such as lymph nodes or the liver, thanks to the emptogenic changes that occur in these cells in primary tumors
said.
," Dr. LaFave said.
new biomarker researchers also compared chromosin states in mouse tumor cells and human lung tumors.
results also showed an increase in the expression of RUNX2 in more aggressive human tumors, suggesting that RUNX2 could be a biomarker for predicting patient prognostics (see figure below).
: Cancer CellRUNX-positive height foreshadows poor survival in lung cancer patients.
, when patients have early RUNX-positive characteristics, they can also be used to better predict patient prognostics.
RUNX may also be a potential drug target, although drugs that target transcription factors are difficult to design (transcription factors often lack a clear structure that can act as a drug binding site).
researchers are also looking for other potential targets in the etogenetic changes identified in more aggressive tumor cells.
these targets may include chromosomal regulatory factors ,a protein responsible for controlling the chemical modification of chromosomals.
" chromosin regulatory factors are usually enzymes and are therefore more likely to be targeted.
we are also exploring what are the key targets driving the transition of these chromoses and which of them are therapeutically targeted.
," Dr. LaFave said.
: 1 s Lindsay M. LaFave et al. EpiGenomic State Transitions Featured Tumor Progression in Mouse Lung Adenocarcinoma. Cancer Cell (2020).2?Gene-controling mechanisms play key role in cancer progression (Source: MIT.com)