How Does Cancer Affect Transcription? Whether in the human body or the plant kingdom, transcription is an essential process in the life cycle of a cell. A disease such as cancer can affect the production of a cell's genes, and if it is not managed correctly, the cells may not function properly. However, there are ways to combat cancer by targeting specific gene sequences, known as 'targeted therapies. During cancer development, transcription factors, such as the epithelial to mesenchymal transition, regulate cell fate decisions. Dysregulation of these factors can lead to abnormal cell differentiation, carcinogenesis, and metastasis. This review aims to summarize the current knowledge of the transcription factor functions in cancer. Specifically, the main goal is to highlight the differences in how these proteins are controlled during tumor development. A linear regression approach was used to determine the associations between TFs and drug classes using various sources. Significant correlations were found between the TFs and drugs for most cancer types studied. The area algorithm from VIPER was used to estimate the relative activity of each TF. The eBay test obtained the corresponding nominal P values. This is a partial list of TFs. The table shows a summary of the most significant TF-related associations. These include oncogenic TFs, drugs for the ERK-MAPK pathway, and drugs targeting cytotoxic pathways. ETFs are also shown to be involved in immune functions in AMLs. A subset of TF regulons, namely, E2F, FOS, and DAF, has been reported to be increased in some cancers. These regulons are believed to be critical nodal oncogenic drivers. However, these regulons are difficult to circumvent by secondary genetic alterations. Several epigenetic mechanisms affect gene expression during cancer development and progression. Among these are DNA methylation and posttranslational histone modifications. These epigenetic changes alter the chromatin structure and result in global dysregulation of gene expression profiles. These changes can also promote tumorigenesis by regulating the activity of tumor suppressor genes and oncogenes. There are four main categories of epigenetic mechanisms, namely: (i) DNA methylation, (ii) histone acetylation, (iii) posttranslational histone modification, and (iv) regulation of non-coding RNAs. These epigenetic processes are reversible and can be reversed by pharmaceuticals. They may be used as complementary or primary treatment options. In addition to gene regulation, chromatin also plays a role in maintaining cellular functions. It consists of 146 base pairs of DNA wrapped around the octamer of four core histone proteins. During development and growth, these histone proteins undergo several posttranslational
covalent modifications. These modifications are carried out by histone acetyltransferases (HATs) and histone deacetylases (HDACs). HDACs work in tandem with HATs to maintain histone acetylation levels. However, abnormal histone acetylation levels can lead to selective inhibition of cancer genes. Various types of cancer have been associated with aberrant DNA methylation. These changes are caused by the interaction of histone marks with the DNA methylation machinery. During the last two decades, many targeted anticancer therapies have been developed. These drugs block signals that cause cancer cells to grow. They can target cancer genes and proteins and are often referred to as molecularly targeted drugs. They are considered to be very safe and effective. However, they must be combined with other targeting agents to achieve the most beneficial effect. These agents target master transcription factors, which are essential in directing the growth of cancer cells. In addition to producing cell division, master transcription factors help control the expression of genes. These drugs were considered highly toxic in the early years of cancer therapy. This was due to a lack of specificity and a vague action mechanism. But recent studies have demonstrated that the effects of these targeted therapies are generally well tolerated. Recently, many targeted therapies have been designed to target DNA repair pathways. These proteins are dysregulated in a wide variety of tumors. The ability of cancer cells to repair therapeutically induced DNA damage has a significant impact on the efficacy of these drugs. Another class of targeted therapies targets angiogenesis inhibitors. These drugs prevent the formation of new blood vessels. This has led to increased treatment doses and increased cure rates.