MicroRNAs (miRNAs) are endogenous ∼23 nt RNAs that play important gene-regulatory roles in animals and plants by pairing to the mRNAs of protein-coding genes to direct their posttranscriptional repression. This review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.

MicroRNAs: Target Recognition and Regulatory Functions

// Yong Wang 1, * , Yueyang Zhang 2, * , Tao Yang 3, * , Wei Zhao 1, * , Ningning Wang 4 , Pengcheng Li 1 , Xiandong Zeng 5 and Weiguo Zhang 3 1 The 4th Department of Orthopedic Surgery, Central Hospital Affiliated to Shenyang Medical College, Shenyang, P. R. China 2 Department of Pathology, Liaoning Cancer Hospital & Institute, Shenyang, P. R. China 3 Department of Joint Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, P. R. China 4 The 2nd Department of Cardiology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, P. R. China 5 Department of Surgical Oncology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, P. R. China * These authors have contributed equally to this work Correspondence to: Yong Wang, email: WY_landy1116@163.com Xiandong Zeng, email: ZXD_landy1116@163.com Keywords: lncRNA MALAT1, miR-144-3p, ceRNA, metastasis and proliferation, osteosarcoma Received: April 26, 2017     Accepted: June 29, 2017     Published: July 31, 2017 ABSTRACT Long non-coding RNAs (lncRNAs) are involved in various biological processes and diseases including osteosarcoma. Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overly expressed in osteosarcoma. But the function and mechanism it works on in osteosarcoma proliferation and metastasis mediated by Rho associated coiled-coil containing protein kinase 1 (ROCK1) and Rho associated coiled-coil containing protein kinase 2 (ROCK2) remain unclear. In the present study, an elevated MALAT1 was found in osteosarcoma tissues and cell lines, and the elevated MALAT1 was correlated with a poor prognosis in osteosarcoma patients. The functional experiments show that a decreased MALAT1 could remarkably inhibit osteosarcoma cell metastasis and proliferation but induce cell cycle arrest, indicating that MALAT1 functioned as an oncogene in osteosarcoma. Furthermore, we confirmed that MALAT1 and ROCK1/ROCK2 which were targeted by microRNA-144-3p (miR-144-3p) shared the same miR-144-3p combining site. Furthermore, the constructed luciferase assay verified that MALAT1 was a target of miR-144-3p. Additionally, the results of a qRT-PCR demonstrated that MALAT1 and miR-144-3p repressed each other’s expression in a reciprocal manner. Finally, we affirmed that an overexpression of MALAT1 inhibited ROCK1/ROCK2 expression and its mediated metastasis and proliferation by working as a competitive endogenous RNA (ceRNA) via miR-144-3p. In summary, the findings of this study based on the ceRNA theory, combining the research foundation of miR-144-3p, ROCK1 and ROCK2, taking MALAT1 as a new point of study, provided new insights into molecular level proliferation reversal and metastasis of osteosarcoma.

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Long non-coding RNA MALAT1 for promoting metastasis and proliferation by acting as a ceRNA of miR-144-3p in osteosarcoma cells

miR-590-3p suppresses cancer cell migration, invasion and epithelial-mesenchymal transition in glioblastoma multiforme by targeting ZEB1 and ZEB2.

The sphingosine kinase-1/sphingosine-1-phosphate axis in cancer: Potential target for anticancer therapy

Zinc finger E-box binding homeobox 2 (ZEB2) is a DNA-binding transcription factor, which is mainly involved in epithelial-to-mesenchymal transition (EMT). EMT is a conserved process during which mature and adherent epithelial-like state is converted into a mobile mesenchymal state. Emerging data indicate that ZEB2 plays a pivotal role in EMT-induced processes such as development, differentiation, and malignant mechanisms, for example, drug resistance, cancer stem cell-like traits, apoptosis, survival, cell cycle arrest, tumor recurrence, and metastasis. In this regard, the understanding of mentioned subjects in the development of normal and cancerous cells could be helpful in cancer complexity of diagnosis and therapy. In this study, we review recent findings about the biological properties of ZEB2 in healthy and cancerous states to find new approaches for cancer treatment.

The crucial role of ZEB2: From development to epithelial-to-mesenchymal transition and cancer complexity.

Thyroid cancer is the most common endocrine malignancy, and its incidence has increased rapidly worldwide. The molecular mechanisms underlying thyroid cancer tumorigenesis still need to be further investigated. MicroRNAs (miRNAs), short RNA molecules of approximately 22 nucleotides in length, play crucial roles in tumorigenesis. In the present study, we found that the expression of miR-144 was significantly down-regulated in thyroid cancer as compared with that in normal thyroid tissues, suggesting that miR-144 may be involved in thyroid cancer tumorigenesis. Moreover, our results showed that restoration of miR-144 in K1 and WRO thyroid cancer cells could suppress the invasion and migration capability of these cells. We also demonstrated that miR-144 suppressed the expression of ZEB1 and ZEB2, two E-cadherin suppressors, by directly binding to their 3'-untranslated regions. Furthermore, restoration of ZEB1 or ZEB2 partially rescued the miR-144-induced inhibition of cell invasion. These data suggest miR-144 function as a tumor suppressor in thyroid cancer.

Down-regulation of miR-144 promotes thyroid cancer cell invasion by targeting ZEB1 and ZEB2.

Purpose
The oncogenic roles of sphingosine kinase 1 (SphK1) in various cancers, including thyroid cancer, have been well demonstrated. However, the microRNAs (miRNAs) associated with the oncogenic roles of SphK1 remain largely unknown.

Zhiwei Xie

Papers

Down-regulation of miR-144 promotes thyroid cancer cell invasion by targeting ZEB1 and ZEB2.

Comprehensive gene and microRNA expression profiling reveals a role for miRNAs in the oncogenic roles of SphK1 in papillary thyroid cancer.