Scientists have found the key to "stopping" cancer cells

Cells are always dividing in the body, and uncontrolled errors in the process can contribute to genetic errors and may continue to develop into cancer cells.
since cancer cells were discovered more than 100 years ago, scientists have been trying to find ways to eliminate these "harmful" cells and cure cancer.
recently, the top journal Nature published two heavyweight articles on cancer treatment.
In this tweet, the editor-in-chief shares the first article, an article by scientists at Oxford University and Johns Hopkins University entitled TargetING TRIM37-driven centrosome dysfunction in 17q23-amplified breast cancer: Killing certain human breast cancer cells by selectively attacking the core of the cell division mechanism, created new inspiration for us to find drugs that destroy cancer cells without harming healthy cells.
Dr Andrew Holland, associate professor of molecular biology and genetics at Johns Hopkins University School of Medicine and one of the co-authors of the report, said: "Some widely used anticancer drugs have killed rapidly dividing cells, but these drugs have obvious drawbacks and can damage healthy cells while killing cancer cells.
the key is how to destroy cancer cells while protecting healthy cells? Because mammalian cell division processes are similar, Holland's team has long tried to find breakthroughs in cell division mechanisms specific to cancer cells.
is an important cytogenetic device in animal cells and the center of internal activity during cell division.
although some cancer cells can proliferate without a central body, the researchers found that there are a number of human breast cancer cells (MCF-7) that rely heavily on the central body for cell division and survival.
in the study, researchers found that centrally dependent breast cancer cells contained 17q23 breast cancer amplifier, an abnormal number of duplicate copies of 3-4-Mb found in about 9 percent of breast cancer cells.
researchers screened TRIM37 from about 40 protein-coded genes in 17q23 amplifications, which have previously been reported to be associated with central body function, and knocking out this gene will lead to the accumulation of substances around the center body of the centerless granulocyte (PCM) and the accelerated assembly of spindle bodies.
previous studies have shown that the protein kinase PLK4 is a target for blocking the growth of invasive breast cancer cells, and that PLK4 inhibitors can destroy the proteins that make up the central protein, leading to central body failure.
researchers added PPK4 inhibitors to normal trim37-level breast cancer cells grown in the lab and found that even if the center of the cancer cells were removed, they could still divide.
if PLC4 inhibitors are added to breast cancer cells at high TRIM37 levels, most cells will stop growing or die.
suggests that the increase in TRIM37 expression is synthetic and lethal under the suppression of PLC4.
subsequent experiments also confirmed this and further demonstrated that the inhibitor selectivity of PLK4 (rather than other kinases) played a key role in over-expression of the synthetic lethal effects of TRIM37 cells.
PLK4 inhibitor selective rather than other kinases are synthesized to kill overexpressed TRIM37 cells in order to study how PLC4 inhibition triggers growth defects in MCF-7 cells, the researchers used a time-lapse microscope to track the growth of cancer cells using and not using PLC4 inhibitors.
results show that, in the absence of the central body, TRIM37 is the negative regulatory factor of the substances around the central body, and the increase of TRIM37 expression affects the assembly of the spindle body, resulting in a sudden change in silk division.
further analysis shows that TRIM37 over-expression inhibits the formation of non-central PCM cooktops, which have micro-tube nucleation capability and are necessary structures for the successful cell division of the lack of central bodies.
The last model that expressed TRIM37's inhibitory PLC4 synthetic lethal effect in 17q23 amplified breast cancer cells, the researchers also found that TRIM37's overexpression increased the frequency of silk division errors by delaying the maturation of the central body and accelerating the separation of the central body as it entered the silky division.
, by adding PPK4 inhibitions that remove the central grain, whether or not the cancer cell has a central body or PCM, it will not be able to organize the pipes that help the DNA divide during cell division.
in summary, this study shows that inhibiting PPK4 or other regulatory factors associated with central replication and assembly is a promising treatment strategy for selective targeting of breast cancer or other tumors driven by 17q23 amplification.
, researchers are looking for other, more stable drugs similar to PPK4 inhibitors and are trying to identify other human cancer cell lineages that are sensitive to these inhibitors.
reference: s1. Targeting TRIM37-driven centrosome dysfunction in 17q23-amplified breast cancer. New way to target some rapidly dividing cancer cells, leavinginginging healthy cells unharmed.