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Review
. 2021 Mar 16:13:2539-2548.
doi: 10.2147/CMAR.S302173. eCollection 2021.

RUNX2 as a promising therapeutic target for malignant tumors

Affiliations
Review

RUNX2 as a promising therapeutic target for malignant tumors

Weizhu Zhao et al. Cancer Manag Res. .

Abstract

The transcription factor runt-related protein 2 (RUNX2) has an important impact on the transformation of bone marrow mesenchymal stem cells to osteoblasts. Further studies have shown that RUNX2 plays a key role in the invasion and metastasis of cancers. RUNX2 is a "key" molecule in the regulatory network comprised of multiple signaling pathways upstream and its target downstream molecules. Due to the complex regulatory mechanisms of RUNX2, the specific mechanism underlying the occurrence, development and prognosis of malignant tumors has not been fully understood. Currently, RUNX2 as a promising therapeutic target for cancers has become a research hotspot. Herein, we reviewed the current literature on the modulatory functions and mechanisms of RUNX2 in the development of malignant tumors, aiming to explore its potential clinical application in the diagnosis, prognosis and treatment of tumors.

Keywords: RUNX2; malignant tumor;; research progress.

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Conflict of interest statement

The authors declare no conflicts of interest for this work and that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Figure 1
Figure 1
Direct or indirect regulation of RUNX2 by miRNAs via the targeting of signaling pathways in BC. In BC, the miRNAs marked in red color play an oncogenic role, their expression levels are down-regulated; the miRNAs marked in black color act as tumor suppressor genes, their expression levels are up-regulated.
Figure 2
Figure 2
PI3K/AKT-dominated signaling pathway regulates RUNX2 in PCa.
Figure 3
Figure 3
Simulation diagram of RUNX2ʹ s regulation mechanism in malignant tumors. The dotted line indicates that further research is required.

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