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Related Concept Videos

lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

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In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
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Abnormal Proliferation

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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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DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

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As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
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Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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Related Experiment Video

Updated: Jan 16, 2026

Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence
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Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence

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Lamin A/C Deficiency Drives Genomic Instability and Poor Survival in Small-Cell Lung Cancer through Increased R-loop

Christopher W Schultz1, Sourav Saha1, Anjali Dhall1

  • 1Developmental Therapeutics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD.

Biorxiv : the Preprint Server for Biology
|October 1, 2025
PubMed
Summary

Lamin A/C (LMNA) loss in small-cell lung cancer causes genome instability by disrupting nuclear pores and RNA export. Low LMNA levels predict poor patient survival, highlighting its role in cancer and aging.

Keywords:
Biological SciencesCell BiologyR-loopsSmall Cell Lung Cancer (SCLC)agingcancerreplication stress

Related Experiment Videos

Last Updated: Jan 16, 2026

Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence
06:23

Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence

Published on: January 17, 2025

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Area of Science:

  • Nuclear biology
  • Cancer research
  • Molecular genetics

Background:

  • Lamin A/C (LMNA) is crucial for nuclear integrity and genome organization.
  • LMNA dysregulation is linked to genomic instability in cancer and aging, but mechanisms are unclear.
  • Small-cell lung cancer (SCLC) exhibits extreme genomic instability.

Purpose of the Study:

  • To investigate the role of LMNA in SCLC.
  • To elucidate the mechanisms by which LMNA affects genome integrity in SCLC.
  • To explore the clinical relevance of LMNA in SCLC.

Main Methods:

  • LMNA depletion experiments in SCLC models.
  • Analysis of R-loop accumulation, replication stress, DNA breaks, and micronuclei formation.
  • Investigation of nuclear pore complex distribution, FG-nucleoporin incorporation, and RNA export.
  • Assessment of LMNA epigenetic regulation by EZH2 during SCLC differentiation.
  • Correlation analysis of LMNA levels with patient survival data.

Main Results:

  • LMNA depletion leads to R-loop accumulation, transcription-replication conflicts, replication stress, DNA breaks, and micronuclei formation.
  • LMNA loss disrupts nuclear pore complex distribution and impairs RNA export.
  • EZH2 epigenetically represses LMNA during SCLC differentiation.
  • Low LMNA expression correlates with significantly worse survival in SCLC patients.

Conclusions:

  • LMNA safeguards genome integrity and influences tumor heterogeneity in SCLC.
  • LMNA's role in nuclear envelope function and RNA export is critical for preventing genomic instability.
  • LMNA represents a potential therapeutic target and prognostic biomarker in SCLC and other aging-related diseases.