Transcription factor 4 expression in circulating tumor cells from castration-resistant prostate cancer
Naoya Nagaya1,2, Geun Taek Lee2, Yan Lu1
1Department of Urology Juntendo University Graduate School of Medicine Tokyo Japan.
Introduction:
Neuroendocrine differentiation is partly caused by antiandrogen therapy and exhibits an androgen receptor-independent growth mechanism. We hypothesized that the expression of transcription factor 4, an inducer of neuroendocrine differentiation, in circulating tumor cells is related to drug resistance in castration-resistant prostate cancer.
Case Presentation:
We evaluate the messenger ribonucleic acid expression of transcription factor 4 in circulating tumor cells from 17 patients with castration-resistant prostate cancer and compared these levels between patients receiving antiandrogen therapies and those who were resistant to antiandrogen therapies and receiving chemotherapies. The expression of transcription factor 4 in circulating tumor cells was significantly higher among patients receiving chemotherapies.
Conclusion:
This study shows that transcription factor 4 is higher in the group of patients who were judged by their physicians to need chemotherapy treatment.
Insights
Transcription factor 4 (TCF4) expression in circulating tumor cells indicates resistance to antiandrogen therapies in castration-resistant prostate cancer, suggesting a need for chemotherapy.
Area of Science:
- Oncology
- Molecular Biology
Background:
- Neuroendocrine differentiation in prostate cancer can be induced by antiandrogen therapy.
- This differentiation involves androgen receptor-independent growth.
- Transcription factor 4 (TCF4) is implicated as an inducer of neuroendocrine differentiation.
Observation:
- Messenger RNA expression of TCF4 was evaluated in circulating tumor cells (CTCs) from 17 castration-resistant prostate cancer patients.
- TCF4 levels were compared between patients on antiandrogen therapy and those resistant to it, receiving chemotherapy.
- Significantly higher TCF4 expression was observed in CTCs of patients receiving chemotherapy.
Findings:
- TCF4 expression in CTCs is elevated in patients with castration-resistant prostate cancer who require chemotherapy.
- This suggests a correlation between TCF4 expression and the transition to a more aggressive, treatment-resistant cancer phenotype.
Implications:
- TCF4 in CTCs may serve as a biomarker for predicting treatment response and guiding therapy selection in castration-resistant prostate cancer.
- Targeting TCF4 could be a potential strategy to overcome antiandrogen resistance and neuroendocrine differentiation.
