Researchers Discover Mystery Behind Key Cancer-Promoting Gene

The mystery behind how a protein, TGF-beta, can prevent cancer from forming and encourage its aggressive growth in human cell, has been discovered by a team of researchers.

The findings could provide a potential target for treatment with the new insight into the cancer mystery that is considered to be a major paradox of cancer biology. TGF-beta is known as a tumor suppressor, which is necessary to keep cells in check and growing normally.

However, at some point, its function flips and it becomes a tumor promoter, fostering aggressive growth and spread of cancer. The researchers identified Bub1 as a key gene involved in regulating TGF-beta receptor.

“Bub1 is well-known for its role in cell division. But this is the first study that links it to TGF-beta. We think this may explain the paradox of TGF-beta as a tumour promoter and a tumour suppressor,” said study director Alnawaz Rehemtulla from University of Michigan Medical School.

“Our data that Bub1 is involved at the receptor level is completely unexpected,” Rehemtulla added. The team of researchers developed a way to screen for genes that regulate the TGF-beta receptor.

TGF-beta is known to play a role in cells developing characteristics of aggressive cancer cells. Researchers also have known that Bub1 is highly expressed in many different types of cancer. When 720 genes from the human genome were screened against lung cancer and breast cancer cells, Bub1 emerged as playing a strong role in TGF-beta signaling.

Bub1 was shown to bind to the TGF-beta receptor and allows it to turn on aggressive cell growth. When the researchers blocked Bub1, it shut down the TGF-beta pathway completely because Bub1 is found in many types of cancer, developing a drug to target it could potentially impact multiple cancers.

“When you look at gene expression in cancer, Bub1 is in the top five. In addition, Bub1 expression levels correlate with outcome in patients with lung and breast cancer. But we never knew why. Now that we have that link, we’re a step closer to shutting down this cycle,” said Rehemtulla.

The study was in Science Signaling, a journal published by the American Association for the Advancement of Science.


One comment

  1. Iron-Related Cancer-Promoting Genes Uncovered. Now, researchers at the University of Michigan Comprehensive Cancer Center have uncovered a key gene Bub1 involved in regulating TGF-beta receptor. Scientists recognize that environmental, hereditary, and biological factors all play important roles in the development of cancer; it is doubtful that one process is involved in the etiology of all cancers. The exact cause of conversion of normal cells into cancerous ones is still not completely understood. An important factor is permanent alteration in the DNA of the cell, which is passed on to subsequent generations, but scientists do not know why some people succumb to a cancer and others do not. Cellular immunity undoubtedly plays some part in one’s ability to stop the growth of cancerous cells; it is believed by some that most persons develop many small cancers in their lifetime but do not develop clinical signs because their defense mechanisms destroy the malignant cells and prevent their replication. Ultimately, the prevention of cancer depends upon knowledge of each person’s risk factors for development of cancer, and that person’s decision to avoid whenever possible those habits and practices that predispose to the disease. Each organ is made up of several different tissue types. Each type of tissue is made up of specific types of cells. Cancer can develop in just about any type of cell in the body. So there is almost always more than one type of cancer that can develop in any one organ. Medical conditions are often related to other diseases and conditions. Iron deficiency can be the result of numerous and multiple causes. In medicine, iron overload indicates accumulation of iron in the body from any cause. Primary tumors always develop at body sites of excessive iron deposits. Local/regional iron overload can be inherited or acquired. Iron disorders are inherited and can be confirmed with genetic testing. At the cellular level, cancer occurs when cellular iron overload affects cellular organelles. There are many types of organelles. Unfortunately, cellular iron overload can chaotically affect DNA, chromosomes, mitochondria, lysosomes, etc. The gene theory of cancer originated with Theodor Boveri’s suggestion in 1914 that cancer could arise from defects in the segregation of chromosomes during cell division. Otto Warburg argued that cancer should be interpreted as a type of mitochondrial disease. Lysosomal alterations are common in cancerous cells. The Father of Oncology recognizes that cancers are caused by iron-related genes or/and iron-related events. Chemical carcinogens, radiation, viruses, old age and some lifestyle factors non-genetically distort iron metabolism and create local/regional deposits within different tissues and organs. Clinical iron-deficiency methods will beat iron-related diseases (cancers).

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