Can Cancer Be Solved By Overexpressing Tumor Suppressor Genes?

Would it be right to say that Cancer(tumor growth) can be controlled if we can detect the defective cell where the growth factor range of the cell is greater than growth inhibition range, and quickly address such cells by modifying their parameters to make sure that the growth-inhibiting factor is more than the growth factor?

Recent success with Gene editing techniques using nanoparticles can help us manage the cell accumulation phenomenon (tumor) and develop solutions for the second leading cause of death.

We could possibly use electrical properties to detect cancer cells. Cancer cells exhibit both lower electrical membrane potentials and lower electrical impedance than normal cells (Cone, 1985; Blad and Baldetorp, 1996; Stern, 1999). According to Cone two of the most outstanding electrical features of cancer cells is that they constantly maintain their membrane potential at a low value and their intracellular concentration of sodium at a high concentration.

The diagram below illustrates that the possible cancer cell is a resultant of gene mutation or replication errors during cell division. Replication of the data contained within the DNA of living cells will probabilistically result in some errors (mutations). Complex error correction and prevention is built into the process and safeguards the cell against cancer. If a significant error occurs, the damaged cell can self-destruct through programmed cell death, termed apoptosis. If the error control processes fail, then the mutations will survive and be passed along to daughter cells. Tumor cells escape apoptosis by strategies such as loss of the TP53 tumor suppressor, or altered expression of pro- and anti-apoptotic regulators or survival signals.

The errors that cause cancer are self-amplifying and compounding, for example:

  • A mutation in the error-correcting machinery of a cell might cause that cell and its children to accumulate errors more rapidly.
  • A further mutation in an oncogene might cause the cell to reproduce more rapidly and more frequently than its normal counterparts.
  • A further mutation may cause loss of a tumor suppressor gene, disrupting the apoptosis signaling pathway and immortalizing the cell.
  • A further mutation in the signaling machinery of the cell might send error-causing signals to nearby cells.

The transformation of a normal cell into cancer is akin to a chain reaction caused by initial errors, which compound into more severe errors, each progressively allowing the cell to escape more controls that limit normal tissue growth. (Wikipedia)

From this defective cells, malignant transformation can occur through the formation of novel oncogenes, the inappropriate over-expression of normal oncogenes, or by the under-expression or disabling of tumor suppressor genes. However, not all cells, that escapes the Apoptosis cycle can lead to tumor growth. For them to grow rapidly, it is important that the growth promoter gene is overexpressed along with underexpressed tumor suppressor gene. Simply explained, the growth promoter acts as a start signal for cell replication and tumor suppressor gene acts as the stop signal. This mechanism helps in maintaining the right amount of cell required.

When in the case of a cancer cell, where the growth promoter gene is overexpressed, the call for replication is frequent. With a underexpressed suppressor gene, the growth is not hindered and hence the accumulation of cells forming a tumor.

Another feature of cancer cells is that they have unique features that make them “immortal” according to some researchers. The enzyme telomerase is used to extend the cancer cell’s life span. While the telomeres of most cells shorten after each division eventually causing the cell to die, telomerase extends the cell’s telomeres. This is a major reason that cancer cells can accumulate over time creating tumors. However, without the growth stimulation signals, the feature by itself cannot add value to the growth of the cell. But Cancer cells that have over expressive oncogenes with the reverse transcriptase enzyme (telomerase) can possess abilities to grow indefinitely.

Characteristic abilities developed by cancers are divided into categories, specifical evasion of apoptosis, self-sufficiency in growth signals, and insensitivity to anti-growth signals. Limitless replicative potential comes from telomerase. Secondary abilities like sustained angiogenesis, metastasis, reprogramming of energy metabolism and evasion of immune destruction can be witnessed only after a certain cancerous mass (tumor) is formed, resulting from the failures of the basic abilities. If the genes are edited to hinder growth (primary abilities), we have little to worry about the secondary abilities of the cancerous cell.

Originally published at on May 5, 2017.