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Related Concept Videos

Cancer Therapies02:49

Cancer Therapies

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Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
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Targeted Cancer Therapies02:57

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
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Feedback Inhibition00:46

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Biochemical reactions are occurring constantly in cells, converting starting substances to different products, usually with the help of enzymes that speed the reactions. Without enzymes, it would take far too long for most reactions to occur to be useful to the cell!
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Enzyme Inhibition01:30

Enzyme Inhibition

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Inhibitors are molecules that reduce enzyme activity by binding to the enzyme. In a normally functioning cell, enzymes are regulated by a variety of inhibitors. Drugs and other toxins can also inhibit enzymes. Some inhibitors bind to the enzyme’s active site, while others inhibit enzymatic activity by binding to other sites on the protein structure.
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Gene Therapy00:59

Gene Therapy

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Gene therapy is a technique where a gene is inserted into a person’s cells to prevent or treat a serious disease. The added gene may be a healthy version of the gene that is mutated in the patient, or it could be a different gene that inactivates or compensates for the patient’s disease-causing gene. For example, in patients with severe combined immunodeficiency (SCID) due to a mutation in the gene for the enzyme adenosine deaminase, a functioning version of the gene can be...
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Inhibition of Cdk Activity02:34

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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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Related Experiment Video

Updated: Jan 21, 2026

Cerenkov Luminescence Imaging CLI for Cancer Therapy Monitoring
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REV1-POL ζ Inhibition and Cancer Therapy.

Toshiyasu Taniguchi1

  • 1Department of Molecular Life Science, Tokai University School of Medicine, Isehara, Kanagawa 259-1193, Japan.

Molecular Cell
|August 10, 2019
PubMed
Summary

A novel inhibitor targeting the REV1-REV7 interaction blocks mutagenic DNA repair, sensitizing cancer cells to cisplatin treatment. This discovery offers a new strategy to enhance chemotherapy efficacy and reduce treatment-induced mutations.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Drug Discovery

Background:

  • Mutagenic translesion DNA synthesis is crucial for cancer cell survival under genotoxic stress.
  • The interaction between REV1 and REV7 proteins is a key component of this pathway.
  • Targeting this interaction presents a potential therapeutic strategy.

Purpose of the Study:

  • To identify and characterize a small-molecule inhibitor targeting the REV1-REV7 interaction.
  • To evaluate the efficacy of this inhibitor in sensitizing cancer cells to cisplatin.
  • To assess the inhibitor's effect on mutagenesis in vitro and in vivo.

Main Methods:

  • Small-molecule screening and characterization.
  • In vitro and in vivo cancer cell-based assays.

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  • Assessment of DNA damage and repair pathways.
  • Mutagenesis assays.

    • Main Results:

    • A novel small-molecule inhibitor specifically targeting the REV1-REV7 interaction was identified.
    • The inhibitor demonstrated significant sensitization of cancer cells to cisplatin in both in vitro and in vivo models.
    • Treatment with the inhibitor led to a reduction in mutagenesis.

    Conclusions:

    • Inhibition of the REV1-REV7 interaction is a viable strategy to enhance cisplatin chemotherapy.
    • This approach can overcome treatment resistance and reduce secondary mutagenic events in cancer therapy.