Journal of Medical Oncology and Therapeutics

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Mini Review - Journal of Medical Oncology and Therapeutics (2024) Volume 9, Issue 1

Oncogenes: The Molecular Switches Behind Tumorigenesis

Kristino Jen*

Institute for Quantitative Biosciences, The University of Tokyo, Japan

*Corresponding Author:
Kristino Jen
Institute for Quantitative Biosciences,
The University of Tokyo, Japan
E-mail:krjen@iqb.u-tokyo.ac.jp

Received: 27-Dec -2023, Manuscript No. JMOT-24-130083; Editor assigned: 29-Dec -2023, PreQC No. JMOT-24-130083 (PQ); Reviewed: 11 -Jan -2024, QC No. JMOT-24-130083; Revised: 14- Jan -2024, Manuscript No JMOT-24-130083 (R); Published: 22- Jan -2024, DOI: 10.35841 /jmot-9.1.186.

Citation: Kristino Jen, Institute for Quantitative Biosciences, The University of Tokyo, Japan. E-mail: krjen@iqb.u-tokyo.ac.jp.

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Introduction
Cancer, a complex and devastating disease, continues to challenge medical science with its intricate mechanisms and elusive treatments. At the heart of cancer development lies a class of genes known as oncogenes. These molecular switches play a pivotal role in regulating cell growth, differentiation, and survival. Understanding their function and dysregulation provides crucial insights into the initiation and progression of various cancers [1].

Oncogenes are a class of genes that, when mutated or activated, promote uncontrolled cell proliferation, a hallmark of cancer. Initially discovered through the study of retroviruses in the early 20th century, oncogenes were found to be normal cellular genes with the potential to induce cancerous transformation. Further research revealed that these genes encode proteins involved in key signaling pathways that regulate fundamental cellular processes [2].

Transcription initiates the process of gene expression, where genetic information encoded in DNA is transcribed into a complementary RNA sequence. The process begins with the unwinding of the DNA double helix, facilitated by enzymes called helicases. This unwinding exposes a segment of the DNA molecule, termed the transcription bubble [3].

Within the transcription bubble, an enzyme called RNA polymerase binds to the DNA at a specific region called the promoter. The promoter region acts as a signal, indicating the start site for transcription and providing a binding site for RNA polymerase. Once bound, RNA polymerase catalyzes the synthesis of RNA from the DNA template, using one of the DNA strands as a template [4].

With the initiation phase complete, the transcription process enters the elongation phase. RNA polymerase moves along the DNA template, unwinding the double helix ahead of it and synthesizing RNA in the 5' to 3' direction. As RNA polymerase progresses, it incorporates ribonucleotides complementary to the DNA template.The growing RNA molecule, known as the primary transcript or pre-mRNA, is an exact complement to the DNA template strand, except that RNA contains uracil (U) instead of thymine (T). As RNA polymerase moves forward, the DNA helix re-forms behind it, ensuring that only a short segment of DNA remains single-stranded at any given time [5].

Transcription concludes with the termination phase, marking the end of RNA synthesis. Termination mechanisms vary between prokaryotes and eukaryotes. In prokaryotes, termination often involves specific sequences in the DNA template that signal RNA polymerase to stop transcription. These sequences may form hairpin loops in the RNA transcript, causing RNA polymerase to dissociate from the DNA template.In eukaryotes, termination is more complex and involves the recognition of termination signals by specialized proteins. Additionally, eukaryotic RNA polymerases require specific termination factors to dissociate from the DNA template and release the newly synthesized RNA molecule [6].

Once transcription is complete, the primary transcript undergoes post-transcriptional processing to produce a mature mRNA molecule ready for translation. This processing involves several steps, including:A modified nucleotide cap is added to the 5' end of the mRNA molecule, which protects it from degradation and facilitates ribosome binding during translation.A polyadenylate (poly-A) tail is added to the 3' end of the mRNA, which aids in mRNA stability and nuclear export [7].

In eukaryotes, introns (non-coding regions) are removed from the primary transcript through a process called splicing, leaving only the exons (coding regions) to form the mature mRNA molecule.These post-transcriptional modifications ensure that the mRNA is properly processed and ready for translation into proteins [8].

DNA transcription is a fundamental process that lies at the heart of gene expression, serving as the bridge between the genetic information stored in DNA and the synthesis of functional molecules necessary for cellular processes. By transcribing specific genes into RNA molecules, cells can produce proteins with diverse functions, including structural components, enzymes, hormones, and regulatory factors [9].

Understanding the intricacies of DNA transcription not only advances our knowledge of fundamental biological processes but also holds significant implications for fields such as genetics, medicine, and biotechnology. Dysregulation of transcription can lead to various diseases, including cancer and genetic disorders, highlighting the importance of deciphering the transcriptional machinery for therapeutic interventions [10].

Conclusion

In essence, DNA transcription is more than just a molecular process—it is the symphony that orchestrates the harmonious expression of life's genetic repertoire, weaving together the intricate melodies of existence

References

  1. Clayton DA. Transcription and replication of mitochondrial DNA. Human reproduction. 2000 ;15(suppl_2):11-7.

Indexed at, Google Scholar, Cross Ref

  1. Lagerwerf S, Vrouwe MG, Overmeer RM,et al. DNA damage response and transcription. DNA repair. 2011 ;10(7):743-50.

Indexed at, Google Scholar, Cross Ref

  1. Pabo CO, Sauer RT. Transcription factors: structural families and principles of DNA recognition. Annual review of biochemistry. 1992 ;61(1):1053-95.

Indexed at, Google Scholar, Cross Ref

  1. Sobell HM. Actinomycin and DNA transcription. Proceedings of the National Academy of Sciences. 1985 ;82(16):5328-31.

Indexed at,  Cross Ref

  1. Friedberg EC. Relationships between DNA repair and transcription. Annual review of biochemistry. 1996 ;65(1):15-42.

Indexed at, Google Scholar, Cross Ref

  1. Suzuki M, Brenner SE, Gerstein M,et al. DNA recognition code of transcription factors. Protein engineering. 1995 ;8(4):319-28.
  2. Falkenberg M, Larsson NG, Gustafsson CM. DNA replication and transcription in mammalian mitochondria. Annu. Rev. Biochem.. 2007 ;76:679-99.

Indexed at, Google Scholar, Cross Ref

  1. Badis G, Berger MF, Philippakis AA,et al. Diversity and complexity in DNA recognition by transcription factors. Science. 2009 ;324(5935):1720-3.

Indexed at, Google Scholar, Cross Ref

  1. Jolma A, Yan J, Whitington T,et al. DNA-binding specificities of human transcription factors. Cell. 2013 ;152(1):327-39.

Indexed at, Google Scholar, Cross Ref

  1. Tsunoda T, Takagi T. Estimating transcription factor bindability on DNA. Bioinformatics (Oxford, England). 1999 ;15(7):622-30.

Indexed at, Google Scholar, Cross Ref

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