Key result
Periprostatic adipose-derived exosomes may drive obesity-related prostate cancer progression via tumorigenic cross-talk.
Why the study?
Investigating feedback mechanisms between prostate cancer and periglandular adipose, and the role of exosomes as mediators, is needed to understand obesity as a risk factor for prostate cancer.
Targeting exosome-mediated communication between prostate cancer and periprostatic fat may offer new therapeutic directions for obese patients with prostate cancer.
Exosome targeting merits investigation in obesity-linked prostate cancer; leaves open whether disrupting this cross-talk improves outcomes.
The molecular mechanisms of obesity-induced cancer progression have been extensively explored because of the significant increase in obesity and obesity-related diseases worldwide. Studies have shown that obesity is associated with certain features of prostate cancer. In particular, bioactive factors released from periprostatic adipose tissues mediate the bidirectional communication between periprostatic adipose tissue and prostate cancer. Moreover, recent studies have shown that extracellular vesicles have a role in the relationship between tumor peripheral adipose tissue and cancer progression. Therefore, it is necessary to investigate the feedback mechanisms between prostate cancer and periglandular adipose and the role of exosomes as mediators of signal exchange to understand obesity as a risk factor for prostate cancer. This review summarizes the two-way communication between prostate cancer and periglandular adipose and discusses the potential role of exosomes as a cross-talk and the prospect of using adipose tissue as a means to obtain exosomes in vitro. Therefore, this review may provide new directions for the treatment of obesity to suppress prostate cancer.
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Feng et al. (2022) conducted a review in Prostate cancer and obesity. Obesity was evaluated. Obesity may exacerbate prostate cancer progression via exosomes released from periprostatic adipose tissue, which mediate bidirectional tumorigenic cross-talk.
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