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Related Concept Videos

Translesion DNA Polymerases02:10

Translesion DNA Polymerases

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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...
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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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Initiation of Translation02:33

Initiation of Translation

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Initiating translation is complex because it involves multiple molecules. Initiator tRNA, ribosomal subunits, and eukaryotic initiation factors (eIFs) are all required to assemble on the initiation codon of mRNA. This process consists of several steps that are mediated by different eIFs.
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Abnormal Proliferation02:23

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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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Negative Regulator Molecules01:23

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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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Restarting Stalled Replication Forks02:37

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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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Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
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High Risk α-HPV E6 Impairs Translesion Synthesis by Blocking POLη Induction.

Sebastian O Wendel1, Jazmine A Snow1, Tyler Bastian2

  • 1Division of Biology, Kansas State University, Manhattan, KS 66506, USA.

Cancers
|December 30, 2020
PubMed
Summary

High-risk human papillomaviruses (α-HPVs) disrupt DNA repair pathways, increasing cervical cancer risk. Restoring the translesion synthesis (TLS) polymerase POLη can overcome treatment resistance by preventing replication fork collapse.

Keywords:
CisplatinCisplatin resistancecervical cancerpolymerase etatranslesion synthesis

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Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
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A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions
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Area of Science:

  • Oncology
  • Molecular Biology
  • Virology

Background:

  • High-risk alpha human papillomaviruses (α-HPVs) encode E6 and E7 oncogenes crucial for cervical cancer development.
  • These oncogenes target tumor suppressors like p53 and RB, and E7 induces replication stress and alters DNA damage responses (DDR).
  • The translesion synthesis (TLS) pathway is vital for mitigating DNA damage and preventing replication fork collapse during replication stress.

Purpose of the Study:

  • To investigate the role of TLS pathway alterations in cervical cancer.
  • To elucidate the mechanism by which α-HPV oncogenes affect TLS polymerases.
  • To explore therapeutic strategies targeting TLS to overcome treatment resistance.

Main Methods:

  • Computational analysis of cervical cancer transcriptomic datasets.
  • In vitro and ex vivo experimental validation.
  • Interrogation of TLS polymerase (POLη) function and regulation by α-HPV16 E6.

Main Results:

  • Cervical cancer datasets showed increased expression of TLS genes, but not essential TLS polymerases.
  • α-HPV16 E6 was found to degrade p53, inhibiting TLS polymerase induction.
  • This inhibition led to increased replication fork collapse and sensitivity to replication stress-inducing agents (UV, Cisplatin).
  • Exogenous POLη addition rescued sensitivity to these treatments.

Conclusions:

  • α-HPVs subvert the TLS pathway, contributing to cervical cancer pathogenesis.
  • α-HPV E6-mediated p53 degradation is a key mechanism for blocking TLS.
  • Targeting TLS, specifically by restoring POLη function, offers a potential strategy to overcome treatment resistance in cervical cancer.