Dear Editor,
A recently published article entitled “Gene expression of insulin receptor, insulin-like growth factor increases and insulin-like growth factor-binding protein-3 reduces with increase in prostate size in benign prostatic hyperplasia” by Karli Sreenivasulu intrigued our interest [Citation1]. In the study, the authors compared serum insulin, PSA, IGF-1, and IGFBP-3 in BPH patients with prostate size less than 30 ml and more than 30 m. They also measured the gene and protein expression levels of insulin receptor in BPH patients with different prostate size. They found that the activation of insulin related signal pathway was associated with larger prostate size in BPH. This finding was very interesting to us to understand the pathogenesis of large-sized prostate among aging males. Nevertheless, there were several suggestions that may improve the study.
First, as we know, the human prostate tissue consists of two parts: endothelium and stroma and relative function proteins which were differently expressed in different prostate sections [Citation2]. The authors did not distinguish protein expression levels of insulin receptor among endothelium and stroma in the BPH tissue although these gene and protein expression levels differed significantly in the total protein samples between small-sized prostate (≤30 ml) and large-sized prostate (>30 ml).
Second, the study found that the serum prostate-specific antigen (PSA) levels were elevated in the patients with large-sized prostate (>30 ml) compared to the patients with small-sized prostate (≤30 ml). We consider that the PSA expression levels in the prostate tissue should be measured. The PSA product lies downstream of androgen receptor (AR) and the large-sized prostate may also be associated with the activation of AR. It was suggested that there was a crosstalk between AR signal and PI3K/AKT signal pathway activated by insulin and IGF-1 [Citation3].
Previously, our research group did a study that supported the increased AR expression in the prostate was associated with large-sized prostates (≥100 ml) [Citation4]. Consequently, we thought that a crosstalk between AR signal and insulin/IGF-1 signal pathway may be one of the pathogenesis of large-sized prostate. The specific mechanism involving in the crosstalk was worthy of study in the future.
Disclosure statement
All authors declare that they have no conflict of interest.
References
- Sreenivasulu K, Nandeesha H, Dorairajan LN, et al. Gene expression of insulin receptor, insulin-like growth factor increases and insulin-like growth factor-binding protein-3 reduces with increase in prostate size in benign prostatic hyperplasia. Aging Male. 2017 [cited Nov 12]. DOI:10.1080/13685538.2017.1401994
- Nicholson TM, Sehgal PD, Drew SA, et al. Sex steroid receptor expression and localization in benign prostatic hyperplasia varies with tissue compartment. Different Res Biol Divers. 2013;85:140–149.
- Wu JD, Haugk K, Woodke L, et al. Interaction of IGF signaling and the androgen receptor in prostate cancer progression. J Cell Biochem. 2006;99:392–401.
- Zhang P, Hu WL, Cheng B, et al. Which play a more important role in the development of large-sized prostates (>/=80 ml), androgen receptors or oestrogen receptors? A comparative study. Int Urol Nephrol. 2016;48:325–333.