Abstract

MicroRNAs (miRNAs) consist of a large family of small, non-coding RNAs with the ability to result in gene silencing post-transcriptionally. With recent advances in research technology over the past several years, the physiological and pathological potentials of miRNAs have been gradually uncovered. MiR-149-5p, a conserved miRNA, was found to regulate physiological processes, such as inflammatory response, adipogenesis and cell proliferation. Notably, increasing studies indicate miR-149-5p may act as an important regulator in solid tumors, especially cancers in reproductive system and digestive system. It has been acknowledged that miR-149-5p can function as an oncogene or tumor suppressor in different cancers, which is achieved by controlling a variety of genes expression and adjusting downstream signaling pathway. Moreover, the levels of miR-149-5p are influenced by several newly discovered long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs). However, there is blank about systematic function and mechanism of miR-149-5p in human cancers. In this review, we firstly summarize the present comprehension of miR-149-5p at the molecular level, its vital role in tumor initiation and progression, as well as its potential roles in monitoring diverse reproductive and digestive malignancies.

Highlights

  • It is widely acknowledged that microRNAs, a type of short (~22 nucleotides), singlestranded non-coding RNA, are reported to regulate cellular proliferation, differentiation, apoptosis, oxidative stress, and autophagy through binding to the 3′-untranslated region (UTR) of target mRNA, thereby causing translational repression or mRNA degradation in animals or plants [1,2,3,4]

  • One study from Carlo Croce’s laboratory identified that miRNAs play an important role in cancer initiation and progression. This pathbreaking study reported that miR-15/16 acts as tumor suppressors in chronic lymphocytic leukemia (CLL), promoting numerous researchers to unveil the nonnegligible role of miRNA in cell proliferation, migration, metastasis, energy metabolism of various cancers [7]

  • MiR-149-5p displays lower expression level in most cancers, but riches in clinical leukemia samples and peripheral blood of patients with lung adenocarcinoma (LUAD), which makes a dual role of miR-1495p in different cancers (Table 1)

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Summary

INTRODUCTION

It is widely acknowledged that microRNAs (miRNAs), a type of short (~22 nucleotides), singlestranded non-coding RNA, are reported to regulate cellular proliferation, differentiation, apoptosis, oxidative stress, and autophagy through binding to the 3′-untranslated region (UTR) of target mRNA, thereby causing translational repression or mRNA degradation in animals or plants [1,2,3,4]. One study from Carlo Croce’s laboratory identified that miRNAs play an important role in cancer initiation and progression. This pathbreaking study reported that miR-15/16 acts as tumor suppressors in chronic lymphocytic leukemia (CLL), promoting numerous researchers to unveil the nonnegligible role of miRNA in cell proliferation, migration, metastasis, energy metabolism of various cancers [7]. With the rapid development of high-throughput sequencing technology, molecular biology and life science, other ceRNAs apart from protein-coding ceRNAs, such as lncRNAs and circRNAs, sharing common MRE, are discovered as important upstream modulators by serving as miRNA sponges, thereby repressing normal miRNA targeting activity on mRNA [9, 10]. We systematically summarize the expression, function, target genes, upstream regulators and application potentials in different cancers, with special emphasis on reproductive system and digestive system cancers

Role of miR-149-5p in Adipogenesis
Role of miR-149-5p in Vascular Smooth Muscle Cells
Other Functions
Cancers of the Reproductive System
Cancers of the Digestive System
Cancers of the Respiratory System
Cancers of the Urinary System
Cancers of the Endocrine System
Cancers of the Circulatory System
Cancers of the Nervous System
Cancers of the Motor System
Findings
CONCLUSION
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