Abstract

MicroRNAs (miRNAs) are small non-coding RNAs that can negatively regulate gene expression at the post-transcriptional level through the RNA-induced silencing complex (RISC)-mediated inhibition. Because of the imperfect and short seed-binding region of the target sequences, miRNAs hold capacity for multi-targeting and are able to regulate a wide range of cellular functions and signaling. Numerous researches have revealed that dysregulated miRNAs are closely associated with cancer progression. Moreover, genome-wide screening shows that the expression profile of miRNAs can serve as biomarkers for early diagnosis, stratifying patient outcome, and predicting treatment efficiency for cancer patients. Hence, seeking and dissecting the detailed mechanisms of cancer-associated miRNA may provide a new avenue for cancer targeting therapy. This review discussed the current proposed mechanisms of miR-135b involvement in cancer progression and tissue differentiation, both of which are considered as functional equivalents. The regulatory network of miR-135b are also addressed to further clarify the potential oncogenic role of miR-135b.

Highlights

  • Several lung cancer-associated miRNAs have recently been identified

  • An up-regulated miR-135b is highly associated with poor overall survival in non-small cell lung cancer (NSCLC)

  • The oncogenic mechanism is via the suppression of LZTS1 and multiple components of the Hippo pathway

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Summary

Introduction

Several lung cancer-associated miRNAs have recently been identified. Among them, miR-135b antisense stands out for its therapeutic potential or its oncogenic role [1,2,3]. An up-regulated miR-135b is highly associated with poor overall survival in non-small cell lung cancer (NSCLC). The various oncogenic functions of miR-135b may be attributed to its multi-targeting ability, which involves different mechanisms during tumor progression. The oncogenic roles of miR-135b on cancer stemness and drug-resistance are yet to be clarified.

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Conclusion
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