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PRC2 mediated KLF2 down regulation: a therapeutic and diagnostic axis during tumor progression
Negin Taghehchian1, Amirhosein Maharati1,2, Iman Akhlaghipour2
1Medical Genetics Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Abstract:
Surgery and chemo-radiotherapy are used as the common first-line treatment options in many cancers. However, tumor relapse is observed in many cancer patients following such first-line treatments. Therefore, targeted therapy according to the molecular cancer biology can be very important in reducing tumor recurrence. In this regard, a wide range of monoclonal antibodies against the growth factors and their receptors can offer more targeted treatment in cancer patients. However, due to the importance of growth factors in the normal biology of body cells, side effects can also be observed following the application of growth factor inhibitors. Therefore, more specific factors should be introduced as therapeutic targets with less side effects. Krüppel-like factors 2 (KLF2) belongs to the KLF family of transcription factors that are involved in the regulation of many cellular processes. KLF2 deregulations have been also reported during the progression of many tumors. In the present review we discussed the molecular mechanisms of KLF2 during tumor growth and invasion. It has been shown that the KLF2 as a tumor suppressor is mainly inhibited by the non-coding RNAs (ncRNAs) through the polycomb repressive complex 2 (PRC2) recruitment. This review is an effective step towards introducing the KLF2 as a suitable diagnostic and therapeutic target in cancer patients.
Insights
Krüppel-like factor 2 (KLF2) acts as a tumor suppressor, often inhibited by non-coding RNAs. Targeting KLF2 could offer a novel therapeutic strategy to reduce cancer recurrence and minimize side effects.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Standard cancer treatments like surgery and chemo-radiotherapy often lead to tumor relapse.
- Targeted therapies, such as monoclonal antibodies, show promise but can cause side effects due to the essential roles of growth factors in normal cells.
- There is a need for more specific therapeutic targets with fewer side effects in cancer treatment.
Purpose of the Study:
- To review the molecular mechanisms of Krüppel-like factor 2 (KLF2) in cancer progression, invasion, and its potential as a therapeutic target.
- To elucidate how non-coding RNAs (ncRNAs) regulate KLF2 function in tumors.
- To highlight KLF2 as a potential diagnostic and therapeutic target for reducing tumor recurrence.
Main Methods:
- Review of existing literature on KLF2 function in cancer.
- Analysis of molecular mechanisms involving KLF2, non-coding RNAs, and the polycomb repressive complex 2 (PRC2).
- Discussion of KLF2's role as a tumor suppressor and its deregulation in various cancers.
Main Results:
- KLF2 functions as a tumor suppressor, and its activity is frequently inhibited by ncRNAs.
- ncRNAs inhibit KLF2 by recruiting the polycomb repressive complex 2 (PRC2).
- Deregulation of KLF2 is implicated in the progression and invasion of numerous tumors.
Conclusions:
- KLF2 is a critical regulator of cellular processes and acts as a tumor suppressor.
- Inhibition of KLF2 by ncRNAs is a key mechanism in tumor development.
- KLF2 represents a promising molecular target for developing novel, specific cancer therapies with potentially reduced side effects.
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