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Updated: Aug 12, 2025

Author Spotlight: Reprogramming Cancer Cells to iPSCs to Study Disease Progression and Treatment Targets
Published on: February 2, 2024
Transcription networks rewire gene repertoire to coordinate cellular reprograming in prostate cancer
Nishat Manzar1, Promit Ganguly1, Umar Khalid Khan1
1Molecular Oncology Laboratory, Department of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, UP, India.
Abstract:
Transcription factors (TFs) represent the most commonly deregulated DNA-binding class of proteins associated with multiple human cancers. They can act as transcriptional activators or repressors that rewire the cistrome, resulting in cellular reprogramming during cancer progression. Deregulation of TFs is associated with the onset and maintenance of various cancer types including prostate cancer. An emerging subset of TFs has been implicated in the regulation of multiple cancer hallmarks during tumorigenesis. Here, we discuss the role of key TFs which modulate transcriptional cicuitries involved in the development and progression of prostate cancer. We further highlight the role of TFs associated with key cancer hallmarks, including, chromatin remodeling, genome instability, DNA repair, invasion, and metastasis. We also discuss the pluripotent function of TFs in conferring lineage plasticity, that aids in disease progression to neuroendocrine prostate cancer. At the end, we summarize the current understanding and approaches employed for the therapeutic targeting of TFs and their cofactors in the clinical setups to prevent disease progression.
Insights
Transcription factors (TFs) are key regulators in cancer, particularly prostate cancer. Targeting these deregulated proteins and their cofactors offers new therapeutic strategies for disease progression.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Transcription factors (TFs) are frequently deregulated in human cancers.
- TF dysregulation drives cellular reprogramming and cancer progression.
- Prostate cancer development and maintenance are linked to TF deregulation.
Purpose of the Study:
- To discuss the role of key TFs in prostate cancer development and progression.
- To highlight TFs involved in cancer hallmarks like chromatin remodeling and metastasis.
- To explore TF functions in lineage plasticity and neuroendocrine prostate cancer.
Main Methods:
- Literature review and synthesis of current research on TFs in prostate cancer.
- Analysis of TF roles in regulating transcriptional circuitries.
- Discussion of TF involvement in cancer hallmarks and therapeutic targeting.
Main Results:
- Specific TFs modulate transcriptional networks crucial for prostate cancer.
- TFs are implicated in chromatin remodeling, genome instability, DNA repair, invasion, and metastasis.
- TFs contribute to lineage plasticity, driving progression to neuroendocrine prostate cancer.
Conclusions:
- TFs are central players in prostate cancer pathogenesis and progression.
- Understanding TF functions provides insights into cancer hallmarks.
- Therapeutic targeting of TFs and cofactors shows promise for clinical intervention.
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