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Crosstalk Between ROS and Autophagy in Tumorigenesis: Understanding the Multifaceted Paradox
Adria Hasan1,2, Suroor Fatima Rizvi1,2, Sana Parveen1,3
1Molecular Cell Biology Laboratory, Integral Information and Research Centre-4 (IIRC-4), Integral University, Lucknow, India.
Abstract:
Cancer formation is a highly regulated and complex process, largely dependent on its microenvironment. This complexity highlights the need for developing novel target-based therapies depending on cancer phenotype and genotype. Autophagy, a catabolic process, removes damaged and defective cellular materials through lysosomes. It is activated in response to stress conditions such as nutrient deprivation, hypoxia, and oxidative stress. Oxidative stress is induced by excess reactive oxygen species (ROS) that are multifaceted molecules that drive several pathophysiological conditions, including cancer. Moreover, autophagy also plays a dual role, initially inhibiting tumor formation but promoting tumor progression during advanced stages. Mounting evidence has suggested an intricate crosstalk between autophagy and ROS where they can either suppress cancer formation or promote disease etiology. This review highlights the regulatory roles of autophagy and ROS from tumor induction to metastasis. We also discuss the therapeutic strategies that have been devised so far to combat cancer. Based on the review, we finally present some gap areas that could be targeted and may provide a basis for cancer suppression.
Insights
Autophagy and reactive oxygen species (ROS) play complex roles in cancer, influencing tumor formation and progression. Understanding their interaction offers new therapeutic targets for cancer suppression.
Area of Science:
- Oncology
- Cellular Biology
Background:
- Cancer development is influenced by the tumor microenvironment and requires targeted therapies.
- Autophagy, a cellular degradation process, is activated by stress and plays a dual role in cancer.
- Reactive oxygen species (ROS) are implicated in various pathophysiological conditions, including cancer.
Purpose of the Study:
- To review the regulatory roles of autophagy and ROS in cancer from induction to metastasis.
- To discuss current therapeutic strategies targeting autophagy and ROS in cancer treatment.
- To identify potential therapeutic gaps for future cancer suppression strategies.
Main Methods:
- Literature review of studies on autophagy, ROS, and cancer.
- Analysis of the interplay between autophagy and ROS in different cancer stages.
- Evaluation of existing and potential therapeutic interventions.
Main Results:
- Autophagy and ROS exhibit a complex, often dual role in cancer, capable of both inhibiting and promoting tumor growth.
- The interaction between autophagy and ROS is crucial in regulating cancer initiation, progression, and metastasis.
- Current therapeutic strategies show promise but highlight the need for further development.
Conclusions:
- Targeting the intricate crosstalk between autophagy and ROS presents a promising avenue for novel cancer therapies.
- Further research into specific molecular mechanisms and therapeutic interventions is needed to fully exploit this relationship for cancer suppression.
- Identifying and addressing current gaps in knowledge can pave the way for more effective cancer treatments.
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