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Unveiling the HSF1 Interaction Network: Key Regulators of Its Function in Cancer.
Snezhana A Vladimirova1, Nadezhda E Kokoreva1, Irina V Guzhova1
1Institute of Cytology of Russian Academy of Sciences, Tikhoretsky Ave. 4, 194064 St. Petersburg, Russia.
Cancers
|December 17, 2024
Summary
Heat shock factor 1 (HSF1) is crucial for cancer cell survival and drug resistance by regulating stress responses. Targeting HSF1 interactions offers new therapeutic strategies for cancer treatment.
Area of Science:
- Molecular Biology
- Oncology
- Cellular Stress Response
Background:
- Heat shock factor 1 (HSF1) orchestrates the heat shock response (HSR), activating heat shock proteins (HSPs) and other genes.
- Cancer cells exhibit proteotoxic stress, leading to constitutive HSR activation and reliance on HSPs for survival.
- HSF1 regulates key cancer processes including proliferation, cell death, drug resistance, immune microenvironment, and cancer stem cells.
Purpose of the Study:
- To review current knowledge on HSF1 interactions in cancer.
- To highlight HSF1's role beyond the HSR in tumor progression.
- To explore HSF1 as a therapeutic target and understand its interactome for novel treatment strategies.
Main Methods:
- Literature review of HSF1's role in cancer.
- Analysis of HSF1's protein-protein interactions (PPIs).
- Summary of HSF1's involvement in gene regulation and cellular functions relevant to cancer.
Main Results:
- HSF1 is a critical regulator of cancer cell adaptation and survival under proteotoxic stress.
- HSF1 interacts with diverse proteins, including chaperones, kinases, and regulators, influencing its activity.
- HSF1's involvement in immune modulation and cancer stem cell maintenance is increasingly recognized.
Conclusions:
- HSF1 is a promising therapeutic target in oncology, with inhibitors in clinical trials.
- Understanding HSF1's extensive interactome is key to developing targeted cancer therapies.
- Disrupting specific HSF1-protein complexes may provide innovative strategies against cancer progression.
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