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Pedersen K, Canals F, Prat A, Tabernero J, Arribas J. Yeast dom34 mutants are defective in multiple developmental pathways and exhibit decreased levels of polyribosomes. Disruption of the Pelota Gene causes early embryonic lethality and defects in cell cycle progression. 2021 40:937вЂ“50.ДЄdham IM, Sallam MA, Steding G, Korabiowska M, Brinck U, Hoyer-Fender S, et al. Bromodomain and extra-terminal motif (BET) inhibition is synthetic lethal with loss of SMAD4 in colorectal cancer cells via restoring the loss of MYC repression. Shi C, Yang EJ, Liu Y, Mou PK, Ren G, Shim JS.

PDK1 signaling toward PLK1вЂ“MYC activation confers oncogenic transformation, tumor-initiating cell activation, and resistance to mTOR-targeted therapy. Tan J, Li Z, Lee PL, Guan P, Aau MY, Lee ST, et al. SMAD4-dependent barrier constrains prostate cancer growth and metastatic progression. Mutat Res/Fundamental Mol Mechanisms Mutagenesis. Therapeutic opportunities for PLK1 inhibitors: Spotlight on BRCA1-deficiency and triple negative breast cancers. GarcГa IA, Garro C, Fernandez E, Soria G. Targeting polo-like kinase 1 for cancer therapy. Polo-like kinase 1 is overexpressed in prostate cancer and linked to higher tumor grades. Weichert W, Schmidt M, Gekeler V, Denkert C, Stephan C, Jung K, et al. Plk1 inhibition enhances the efficacy of androgen signaling blockade in castration-resistant prostate cancer. Zhang Z, Hou X, Shao C, Li J, Cheng J-X, Kuang S, et al. Polo-like Kinase 1 facilitates loss of pten tumor suppressor-induced prostate cancer formation. Liu XS, Song B, Elzey BD, Ratliff TL, Konieczny SF, Cheng L, et al. Prostate-specific markers to identify rare prostate cancer cells in liquid biopsies.

Van der Toom EE, Axelrod HD, de la Rosette JJ, de Reijke TM, Pienta KJ, Valkenburg KC. Targeting FOXA1-mediated repression of TGF-ОІ signaling suppresses castration-resistant prostate cancer progression. Song B, Park S-H, Zhao JC, Fong K, Li S, Lee Y, et al. Overall, these findings identified a novel regulatory relationship among PLK1, Smad4 and PELO, and provided a potential therapeutic strategy for advanced PCa therapy by co-targeting PLK1 and PELO. In addition, blocking the interaction between PELO and Smad4 by using specific peptide could effectively inhibit PCa cell metastasis ability in vitro and vivo. PELO knockdown in PCa cells could enhance the tumor suppressive role of PLK1 inhibitor. Further studies showed that PELO upregulation was positively associated with high grade PCa and knockdown of PELO expression significantly decreased PCa cell proliferation and metastasis in vitro and vivo. Changes in protein levels of Smad4 led to the alteration of biological function that caused by PLK1 in prostate cancer cells. PELO facilitated the degradation of Smad4 through cooperating with PLK1, thereby resulting in proliferation and metastasis of prostate cancer cell. PLK1 and PELO could bind to different domains of Smad4 and formed a protein complex. Here, we showed that PLK1 could interact with Smad4 and promote the ubiquitination and degradation of Smad4 in PCa cells. However, the connections between PLK1 and Smad4 have never been studied. Moreover, they could reversely regulate the PI3K/AKT/mTOR pathway and the activation of MYC. They have been reported to play the opposite role in Pten-deleted mice, one is an oncogene, the other is a tumor suppressor. PLK1 and Smad4 are two important factors in prostate cancer initiation and progression.

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