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Re: The expression of YAP1 is increased in high-grade prostatic adenocarcinoma but is reduced in neuroendocrine prostate cancer

Prostate Cancer and Prostatic Diseases volume 24, pages 1212–1213 (2021)Cite this article

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Recently, we ready the paper of Cheng et al. about the alteration of YAP1 expression during prostate cancer progression [1]. They demonstrated the expression of YAP1 is increased in high-grade prostate adenocarcinomas while lost in neuroendocrine prostate cancer (NEPC) [1]. And they proposed the hypothesis that the change of Wnt/β-Catenin pathway may contribute to this process [1].

This is an amazing research. However, we think the authors could do some further research. First, in the research of Dr. Huang’s team, they compared the LNCap and PC3 cell lines, PC3 without the expression of androgen receptor (AR) and prostate-specific antigen (PSA), and their growth is not inhibited by castration treatment, similar to human prostatic adenocarcinoma [2]. And the PC3 xenograft tumor tissue show some morphological specifics of small cell. While LNCap express AR and PSA, and their proliferation is unindependent of androgen withdrawal similar to adenocarcinoma [2]. NEPC and PC3 cells are positive for neuroendocrine markers (Chromogranin A [Cg A] and Neuron-specific enolase [NSE]) and stem cell-associated marker CD44 while adenocarcinoma cells and LNCap cells are negative [2]. LNCap cells have identical cytokeratin profiles to adenocarcinoma while PC3 cells have cytokeratin profiles similar to NEPC [2]. Above all, the PC3 should also be considered as an NEPC cell line. However, the YAP1 can be found at this cell line [1], so it is controversial to say the YAP1 loss is related to NEPC. So we recommend the authors take further explore at the other NEPC cell lines to provide more evidences, like the LASCPC-01 [3]. And authors also demonstrated the YAP1 express increased when the Gleason Score improved in adenocarcinoma [1].However the NE markers also elevated in this process [4,5,6]. If the YAP1 lost related to NEPC as authors proposed, the NE markers should decline; Second, Bekir Cinar et al. demonstrated that YAP1 is a physiological binding partner and positive regulator of AR in prostate cancer [7]. So the authors proposed that the YAP1 lost at the NEPC cells in mice tumor tissues [1], maybe better considered as an explaining of the AR loss in those cells, instead of an evidence of YAP1 related to neuroendocrine differentiation (NED). Third, about the mechanism explore, authors proposed the Wnt/β-Catenin pathway changed after the YAP1 knockdown may contribute to the NED, but significant changes in the expression of NEPC markers failed to be detected [1]. Meanwhile, some paper reported the association between Wnt/β-Catenin pathway and AR expression [8, 9], so this pathway may play the role in AR expression rather than NED. Moreover, the author also found YAP1 can regulate the PI3K/AKT path way [1], which is associated to the AR express [10]. So we recommend the authors should focus on the YAP1 and AR, instead of NED.

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References

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Authors and Affiliations

  1. Department of Pediatrics, Sichuan Tianfu New Area People’s Hospital, Chengdu, China

    Mei Yang, Na Li & Hua Guo

  2. Department of Urology, Sichuan Tianfu New Area People’s Hospital, Chengdu, China

    Jingui Li

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Correspondence to Hua Guo.

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Yang, M., Li, J., Li, N. et al. Re: The expression of YAP1 is increased in high-grade prostatic adenocarcinoma but is reduced in neuroendocrine prostate cancer. Prostate Cancer Prostatic Dis 24, 1212–1213 (2021). https://doi.org/10.1038/s41391-021-00384-7

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