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Related Concept Videos

Telomeres and Telomerase02:41

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In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded...
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Gene expression can be regulated at almost every step from gene to protein. Transcription is the step that is most commonly regulated. This involves the binding of proteins to short regulatory sequences on the DNA. This association can either promote or inhibit the transcription of a gene associated with the respective sequence.
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The gene expression in cells is regulated at different stages: (i) transcription, (ii) RNA processing, (iii) RNA localization, and (iv) translation. Transcriptional regulation is mediated by regulatory proteins such as transcription factors, activators, or repressors—these control gene expression by initiating or inhibiting the transcription of genes. Once a precursor or pre-mRNA is produced, it undergoes post-transcriptional modification, including 5' capping, splicing, and the...
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Guanine nucleotide-binding proteins (G-proteins), also known as GTPases, are a superfamily of proteins that regulate many cellular processes, such as cell signaling, vesicular transport, and the regulation of cell shape and motility. Mutation or dysfunction of these proteins can lead to disease. There are around 40,000 known G-proteins that can broadly be classified into two groups ‒  small G-proteins consisting of a single domain and large multi-domain G-proteins.
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Related Experiment Video

Updated: Jan 22, 2026

Generation of Cancer Cell Clones to Visualize Telomeric Repeat-containing RNA TERRA Expressed from a Single Telomere in Living Cells
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Multiple cancer pathways regulate telomere protection.

Leire Bejarano1, Giuseppe Bosso1, Jessica Louzame1

  • 1Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Centre (CNIO), Madrid, Spain.

EMBO Molecular Medicine
|July 6, 2019
PubMed
Summary

Targeting the shelterin complex, specifically TRF1, shows promise against aggressive cancers. Inhibiting Ras pathway kinases like ERK and MEK mimics TRF1 deletion effects, offering new therapeutic strategies for glioblastoma.

Keywords:
ERK kinaseTRF1 inhibitorsdrug resistanceglioblastomatelomeres

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Telomeres are crucial for cancer cell proliferation, making them a key anti-cancer target.
  • While telomerase inhibition is common, targeting the shelterin complex offers a novel strategy.
  • TRF1, an essential shelterin protein, has been shown to impair tumor growth when genetically deleted.

Purpose of the Study:

  • To screen for drugs inhibiting TRF1 function.
  • To identify novel drug combinations targeting TRF1 for cancer therapy.
  • To explore TRF1 regulation by kinases and its role in cancer stemness.

Main Methods:

  • Screening FDA-approved and clinical trial drugs for TRF1 inhibition.
  • Utilizing aggressive lung cancer and glioblastoma (GBM) mouse models.
  • Investigating kinase-mediated phosphorylation of TRF1 in vitro and in vivo.
  • Testing drug combinations in patient-derived glioblastoma xenograft models.

Main Results:

  • Inhibition of Ras pathway kinases (ERK, MEK) mimics TRF1 genetic deletion effects.
  • TRF1 inhibition induces telomeric DNA damage, telomere fragility, and reduces cancer stemness.
  • bRAF and ERK2 kinases phosphorylate TRF1, regulating its telomere localization.
  • Novel drug combinations targeting TRF1 pathways show potential in blocking resistance.

Conclusions:

  • Targeting TRF1 and its regulatory kinases presents a promising strategy against aggressive cancers like GBM.
  • Inhibiting Ras pathway kinases offers a viable alternative to direct TRF1 inhibition.
  • Combination therapies based on TRF1 inhibition may overcome drug resistance in cancer patients.