Cancer cells fighting against DNA damage and proteasome inhibitors.

Can Proteasome Inhibitors Stop Cancer?

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Jordan Keane in Health & Wellness June 2025 • 4 min read.

"New research explores how proteasome inhibition prevents cell death in cisplatin-treated cells, offering potential breakthroughs in cancer treatment strategies."


Cisplatin, a potent chemotherapy drug, is a cornerstone in the treatment of various cancers. It acts by damaging the DNA of rapidly dividing cancer cells, triggering a cascade of events that lead to cell death. However, the development of resistance to cisplatin remains a significant hurdle in cancer therapy, leading researchers to explore new strategies to enhance its effectiveness and overcome resistance mechanisms.

One promising avenue of research involves proteasome inhibitors. Proteasomes are cellular machines responsible for breaking down unwanted or damaged proteins. By inhibiting proteasomes, researchers aim to disrupt the cellular processes that contribute to cancer cell survival. Recent studies have investigated how proteasome inhibition can influence the effectiveness of cisplatin and whether it can help prevent cancer cells from developing resistance.

Researchers have focused on understanding the intricate relationship between proteasome inhibition and cisplatin treatment. The study sheds light on the mechanisms by which proteasome inhibitors can prevent cell death induced by cisplatin, potentially opening new doors for cancer treatment.

Understanding Proteasome Inhibition and Cisplatin: A New Approach to Cancer Treatment

Cancer cells fighting against DNA damage and proteasome inhibitors.

The research highlights the role of proteasome inhibition in preventing cell death induced by cisplatin. This finding suggests that proteasome inhibitors could enhance the efficacy of cisplatin by preventing cancer cells from surviving the DNA damage caused by the drug. This approach could be particularly useful in cancers that have developed resistance to cisplatin.

The study found that proteasome inhibition does not affect the DNA damage response induced by cisplatin. This is significant because it indicates that proteasome inhibitors are acting downstream of DNA damage, influencing the cell's decision to undergo cell death rather than preventing the initial damage. This insight helps refine the understanding of how proteasome inhibitors work in conjunction with cisplatin.

  • Proteasome Inhibition Prevents Cell Death: Protects against cisplatin-induced cell death but not MMS-induced cell death in yeast.
  • Unique Mechanism: Unlike cisplatin, MMS does not induce active cell death in yeast.
  • Unaffected DNA Damage Response: The proteasome does not alter the DNA damage response caused by cisplatin.
  • Downstream Function: Proteasome inhibition functions downstream of cisplatin-induced DNA damage.
Researchers used yeast cells as a model to study the effects of proteasome inhibition on cisplatin-induced cell death. This model allowed them to identify the specific mechanisms involved in the process. The researchers found that proteasome inhibition functions downstream of DNA damage, influencing the cell's decision to undergo cell death. Elucidating these mechanisms will aid in developing new strategies to increase the efficacy of chemotherapy.

Future Directions and Implications

The insights from this study pave the way for new research directions in cancer therapy. By understanding how proteasome inhibitors interact with cisplatin, researchers can develop more effective combination therapies that overcome cisplatin resistance and improve patient outcomes. These advancements could lead to more personalized and targeted treatments, ultimately enhancing the quality of life for cancer patients. Further research is needed to translate these findings into clinical applications, but the initial results are promising.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1016/j.dnarep.2018.10.006, Alternate LINK

Title: Proteasome Inhibition Prevents Cell Death Induced By The Chemotherapeutic Agent Cisplatin Downstream Of Dna Damage

Subject: Cell Biology

Journal: DNA Repair

Publisher: Elsevier BV

Authors: Ana Rita Costa, Nuno Machado, António Rego, Maria João Sousa, Manuela Côrte-Real, Susana R. Chaves

Published: 2019-01-01

Everything You Need To Know

1

What are proteasome inhibitors, and what do they do?

Proteasomes are cellular machines responsible for breaking down unwanted or damaged proteins. By inhibiting these proteasomes, researchers aim to disrupt cellular processes that contribute to cancer cell survival. The inhibition has been shown to prevent cell death in cancer cells treated with Cisplatin, potentially enhancing the efficacy of this chemotherapy drug.

2

What is Cisplatin, and why is it important in cancer treatment?

Cisplatin is a potent chemotherapy drug used in the treatment of various cancers. It works by damaging the DNA of rapidly dividing cancer cells, leading to cell death. However, resistance to Cisplatin can develop, which is a significant hurdle in cancer therapy. This is where the role of proteasome inhibitors becomes crucial as they are being studied to overcome Cisplatin resistance.

3

How do proteasome inhibitors interact with Cisplatin in cancer treatment?

Proteasome inhibitors prevent cell death induced by Cisplatin. The research indicates that these inhibitors do not affect the DNA damage response caused by Cisplatin. They function downstream of DNA damage, influencing the cell's decision to undergo cell death. This understanding could lead to more effective combination therapies to overcome Cisplatin resistance and improve patient outcomes.

4

What model was used to study this interaction, and what were the key findings?

Researchers used yeast cells to study the effects of proteasome inhibition on Cisplatin-induced cell death. This allowed them to identify specific mechanisms. The research found that proteasome inhibition functions downstream of DNA damage, impacting the cell's decision to die. Elucidating these mechanisms will aid in developing new strategies to increase the efficacy of chemotherapy.

5

What are the potential implications of these findings for the future of cancer treatment?

The study's findings have implications for future cancer therapy. Researchers can develop more effective combination therapies that overcome Cisplatin resistance and improve patient outcomes. This could lead to more personalized and targeted treatments, ultimately enhancing the quality of life for cancer patients. Further research is needed to translate these findings into clinical applications, but the initial results are promising.

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