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Splicing is the process by which eukaryotic RNA is edited before its translation into protein. The RNA strand transcribed from eukaryotic DNA is called the primary transcript. The primary transcripts that become mRNAs are called precursor messenger RNAs (pre-mRNAs). Eukaryotic pre-mRNA contains alternating sequences of exons and introns. Exons are nucleotide sequences that code for proteins, whereas introns are the non-coding regions. In RNA splicing, introns are removed and exons are bonded...
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RNA Polymerase (RNAP) is conserved in all animals, with bacterial, archaeal, and eukaryotic RNAPs sharing significant sequence, structural, and functional similarities. Among the three eukaryotic RNAPs, RNA Polymerase II is most similar to bacterial RNAP in terms of both structural organization and folding topologies of the enzyme subunits. However, these similarities are not reflected in their mechanism of action.
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Noncoding RNA genes in cancer pathogenesis.

Yuri Pekarsky1, Carlo M Croce1

  • 1Department of Cancer Biology and Genetics, The Wexner Medical Center, Columbus, OH, USA.

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|January 7, 2019
PubMed
Summary
This summary is machine-generated.

Researchers found that most chronic lymphocytic leukemia (CLL) cases involve deletions of miR-15a/miR-16-1, leading to BCL2 overexpression and leukemia. This explains CLL sensitivity to venetoclax and ROR1 targeting, offering new therapeutic strategies.

Keywords:
BCL2CLLROR1miR-15/16tRNA derived fragmentstsRNA

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Chronic lymphocytic leukemia (CLL) pathogenesis involves genetic alterations.
  • MicroRNAs (miRNAs) play crucial roles in cancer development.
  • Specific miRNA deletions are implicated in leukemia progression.

Purpose of the Study:

  • To investigate the role of miR-15a and miR-16-1 in CLL.
  • To identify targets of miR-15/16 in leukemia.
  • To explore novel therapeutic strategies for CLL.

Main Methods:

  • Analysis of genetic deletions in CLL patients.
  • Investigating the regulatory relationship between miR-15/16 and BCL2.
  • Identifying other protein targets of miR-15/16 in CLL.
  • Assessing sensitivity to venetoclax and anti-ROR1 antibodies.

Main Results:

  • The majority of CLL cases (75-85%) exhibit deletion of miR-15a and miR-16-1 at 13q14.
  • miR-15/16 are negative regulators of the BCL2 oncogene; their loss leads to BCL2 overexpression.
  • ROR1, an embryonal antigen, is also regulated by miR-15/16 and overexpressed in ~90% of CLL.
  • CLL cells are sensitive to venetoclax and anti-ROR1 antibodies, with synergistic effects observed.

Conclusions:

  • Deletion of miR-15a/miR-16-1 is a key event in CLL pathogenesis, causing BCL2 overexpression.
  • ROR1 is a novel target of miR-15/16 in CLL, presenting a therapeutic target.
  • Combined targeting of BCL2 with venetoclax and ROR1 with monoclonal antibodies shows synergistic efficacy in eliminating CLL cells.