Abstract

E2F transcription factor 3 (E2F3) is oncogenic in tumorigenesis. Alterations in E2F3 functions correspond with poor prognosis in various cancers, underscoring their status for the clinical cancer phenotype. Latest reports discovered intricate networks between microRNAs (miRNAs) and E2F3 in regulating the balance of these events, including proliferation, apoptosis, metastasis, as well as drug resistance. miRNAs are non-coding small RNAs which negatively regulate gene expressions post-transcriptionally mainly through 3′-UTR binding of target mRNAs. Increasing evidence shows that E2F3 can be activated/inhibited by numerous miRNAs whose dysregulation has been implicated in malignancy. In turn, miRNAs themselves can be transcriptionally regulated by E2F3, thus forming a negative feedback loop. These findings add a new challenging layer of complexity to E2F3 network. Current understanding of the reciprocal link between E2F3 and miRNAs in human cancers were summarized, which could help to develop potential therapeutic strategies.

Highlights

  • E2F transcription factor 3 (E2F3) belongs to E2F family and has two distinct isoforms, E2F3a and E2F3b, functioning through binding of DP interaction partner proteins [1]

  • We briefly summarized the bidirectional interactions between E2F3 and miRNAs in human cancers

  • Many miRNAs can restrain the activity of E2F3 family members, and E2F3 can in turn regulate many different miRNAs, which play roles in various biological processes that are intertwined with the control of tumor pathogenesis and progression

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Summary

Introduction

E2F transcription factor 3 (E2F3) belongs to E2F family and has two distinct isoforms, E2F3a and E2F3b, functioning through binding of DP interaction partner proteins [1]. Migration, and invasion and induce cell apoptosis miR-200c Bladder cancer Xq26.3, miR-503 was an intragenic miRNA clustered with miR-424, which was significantly decreased in HCC and colorectal cancer (CRC) and functioned as a tumor suppressor by directly targeting E2F3 [48, 49].

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