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. 2024 Jul;397(7):4911-4925.
doi: 10.1007/s00210-023-02928-1. Epub 2024 Jan 2.

PDE3B regulates KRT6B and increases the sensitivity of bladder cancer cells to copper ionophores

Yuankang Feng #  1 , Zhenlin Huang #  1 , Liang Song #  1 , Ningyang Li  1 , Xiang Li  1 , Huihui Shi  2 , Ruoyang Liu  1 , Fubo Lu  1 , Xu Han  1 , Yafei Ding  1 , Yinghui Ding  1   3 , Jun Wang  1 , Jinjian Yang  4 , Zhankui Jia  5
Affiliations

PDE3B regulates KRT6B and increases the sensitivity of bladder cancer cells to copper ionophores

Yuankang Feng et al. Naunyn Schmiedebergs Arch Pharmacol. 2024 Jul.

Abstract

Cuproptosis is a new Cu-dependent programmed cell death manner that has shown regulatory functions in many tumor types, however, its mechanism in bladder cancer remains unclear. Here, we reveal that Phosphodiesterase 3B (PDE3B), a cuproptosis-associated gene, could reduce the invasion and migration of bladder cancer. PDE3B is downregulated in bladder cancer tissues, which is correlated with better prognosis. Conversely, overexpression of PDE3B in bladder cancer cell could significantly resist invasion and migration, which is consistent with the TCGA database results. Future study demonstrate the anti-cancer effect of PDE3B is mediated by Keratin 6B (KRT6B) which leads to the keratinization. Therefore, PDE3B can reduce KRT6B expression and inhibit the invasion and migration of bladder cancer. Meanwhile, increased expression of PDE3B was able to enhance the sensitivity of Cuproptosis drug thiram. This study show that PDE3B/KRT6B is a potential cancer therapeutic target and PDE3B activation is able to increase the sensitivity of bladder cancer cells to copper ionophores.

Keywords: Bladder cancer; Cuproptosis; Epithelial–mesenchymal transition; PDE3B; Thiram.

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