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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Comparison of Three Different Methods for Determining Cell Proliferation in Breast Cancer Cell Lines
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[Full and D-Box-Deficient PTTG1 Isoforms: Effects on Cell Proliferation].

D E Demin1,2, E M Stasevich3, M M Murashko1

  • 1Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119991 Russia.

Molekuliarnaia Biologiia
|December 7, 2022
PubMed
Summary
This summary is machine-generated.

Minor securin (PTTG1) isoforms lacking the D-box significantly impact cell proliferation. Selective knockdown of short PTTG1 mRNA drastically reduced cell growth, highlighting the importance of these understudied isoforms.

Keywords:
D-boxPTTG1cell proliferationminor isoformoncogenesecurin

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Context:

  • Human securin (PTTG1) is a protooncogene upregulated in various cancers.
  • A minor short isoform of securin, lacking exons 3 and 4 (the D-box), was previously identified.
  • The D-box is crucial for recognition by the anaphase-promoting complex (APC/C).

Purpose:

  • To investigate the functional impact of PTTG1 isoforms on cell proliferation.
  • To determine the effects of selective overexpression and knockdown of securin isoforms.
  • To identify other genes with similar alternatively spliced isoforms lacking D-boxes.

Summary:

  • Overexpression of both full-length and short PTTG1 isoforms accelerated cell growth.
  • Selective knockdown of the short PTTG1 isoform mRNA significantly inhibited cell proliferation.
  • Analysis of the GENCODE database revealed 54 additional genes with D-box-lacking isoforms, suggesting a new class of alternative splicing.

Impact:

  • Establishes the critical role of minor PTTG1 isoforms in regulating cell growth.
  • Suggests that alternative splicing, particularly the generation of D-box-lacking isoforms, is a widespread regulatory mechanism.
  • Provides new targets for cancer therapy by highlighting the significance of previously overlooked gene isoforms.