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In Vitro Selection of Engineered Transcriptional Repressors for Targeted Epigenetic Silencing

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Therapeutic targeting of replicative immortality.

Paul Yaswen¹, Karen L MacKenzie², W Nicol Keith³

¹Life Sciences Division, Lawrence Berkeley National Lab, Berkeley, CA, United States.

Seminars in Cancer Biology

|April 15, 2015

Summary

Cancer cells

Keywords:

Oncogenic stress Senescence Telomerase p53 pRB

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Area of Science:

Oncology
Cell Biology
Cancer Therapeutics

Background:

Malignant cells exhibit continuous proliferation, acquiring aberrations for growth and resistance.
Cellular mechanisms, including senescence, act as a hedge against malignant progression.
Senescence, a state of persistent cytostasis, can be triggered by intrinsic or extrinsic factors.

Purpose of the Study:

To explore the role of senescence in cancer therapy.
To investigate novel therapeutic strategies targeting cancer cell senescence.
To evaluate the potential benefits and caveats of senescence-inducing therapies.

Main Methods:

Review of intrinsic and extrinsic triggers of senescence.
Analysis of tumor suppressor pathways (p53, p16/pRB) in senescence induction.
Examination of targeted therapies (CDK inhibitors, PI3K pathway) for cancer cell senescence.

Main Results:

Senescence induction often requires lower drug doses than outright cell death.
Targeted therapies can induce senescence by circumventing tumor suppressor defects or exploiting cancer-specific pathways.
Senescence-inducing treatments may offer improved survival with fewer side effects than conventional chemotherapy.

Conclusions:

Senescence is a promising strategy for cancer treatment, potentially offering reduced toxicity.
Caveats include senescence reversibility, genomic instability, and paracrine effects.
Agents disrupting replicative immortality are valuable for combinatorial cancer therapy.