Next Article in Journal
The Future of Immunotherapy-Based Combination Therapy in Metastatic Renal Cell Carcinoma
Next Article in Special Issue
BRG1 Activates Proliferation and Transcription of Cell Cycle-Dependent Genes in Breast Cancer Cells
Previous Article in Journal
Mutant IDH1 Depletion Downregulates Integrins and Impairs Chondrosarcoma Growth
Previous Article in Special Issue
Immunological Effects of Epigenetic Modifiers

SMYD3: An Oncogenic Driver Targeting Epigenetic Regulation and Signaling Pathways

Department of Biosciences, Università degli Studi Milano, Via Celoria 26, 20133 Milan, Italy
Faculty of Bioscience and Agro-Food and Environmental Technology, University of Teramo, 64100 Teramo, Italy
Medical Genetics, National Institute of Gastroenterology, ‘S. de Bellis’ Research Hospital, Via Turi 27, Castellana Grotte, 70013 Bari, Italy
Division of Medical Genetics, Department of Biomedical Sciences and Human Oncology (DIMO), University of Bari Aldo Moro, Piazza G. Cesare 11, 70124 Bari, Italy
Author to whom correspondence should be addressed.
Cancers 2020, 12(1), 142;
Received: 2 December 2019 / Revised: 26 December 2019 / Accepted: 1 January 2020 / Published: 6 January 2020
(This article belongs to the Special Issue Epigenetic Dysregulation in Cancer: From Mechanism to Therapy)
SMYD3 is a member of the SMYD lysine methylase family and plays an important role in the methylation of various histone and non-histone targets. Aberrant SMYD3 expression contributes to carcinogenesis and SMYD3 upregulation was proposed as a prognostic marker in various solid cancers. Here we summarize SMYD3-mediated regulatory mechanisms, which are implicated in the pathophysiology of cancer, as drivers of distinct oncogenic pathways. We describe SMYD3-dependent mechanisms affecting cancer progression, highlighting SMYD3 interplay with proteins and RNAs involved in the regulation of cancer cell proliferation, migration and invasion. We also address the effectiveness and mechanisms of action for the currently available SMYD3 inhibitors. The findings analyzed herein demonstrate that a complex network of SMYD3-mediated cytoplasmic and nuclear interactions promote oncogenesis across different cancer types. These evidences depict SMYD3 as a modulator of the transcriptional response and of key signaling pathways, orchestrating multiple oncogenic inputs and ultimately, promoting transcriptional reprogramming and tumor transformation. Further insights into the oncogenic role of SMYD3 and its targeting of different synergistic oncogenic signals may be beneficial for effective cancer treatment. View Full-Text
Keywords: SMYD3; KMT; epigenetic inhibitors; lysine methylation SMYD3; KMT; epigenetic inhibitors; lysine methylation
Show Figures

Figure 1

MDPI and ACS Style

Bottino, C.; Peserico, A.; Simone, C.; Caretti, G. SMYD3: An Oncogenic Driver Targeting Epigenetic Regulation and Signaling Pathways. Cancers 2020, 12, 142.

AMA Style

Bottino C, Peserico A, Simone C, Caretti G. SMYD3: An Oncogenic Driver Targeting Epigenetic Regulation and Signaling Pathways. Cancers. 2020; 12(1):142.

Chicago/Turabian Style

Bottino, Cinzia, Alessia Peserico, Cristiano Simone, and Giuseppina Caretti. 2020. "SMYD3: An Oncogenic Driver Targeting Epigenetic Regulation and Signaling Pathways" Cancers 12, no. 1: 142.

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop