MiR-145 in cancer therapy resistance and sensitivity: A comprehensive review - PubMed (original) (raw)

Review

. 2020 Sep;111(9):3122-3131.

doi: 10.1111/cas.14517. Epub 2020 Jul 8.

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Review

MiR-145 in cancer therapy resistance and sensitivity: A comprehensive review

Wenxiu Xu et al. Cancer Sci. 2020 Sep.

Abstract

MircoRNA (miRNA) are a group of small, non-coding, regulatory RNA with an average length of approximately 22 nucleotides, which mostly modulate gene expression post-transcriptionally through complementary binding to the 3'-untranslated region (3'-UTR) of multiple target genes. Emerging evidence has shown that miRNA are frequently dysregulated in a variety of human malignancies. Among them, microRNA-145 (miR-145) has been increasingly identified as a critical suppressor of carcinogenesis and therapeutic resistance. Resistance to tumor therapy is a challenge in cancer treatment due to the daunting range of resistance mechanisms. We reviewed the status quo of recent advancements in the knowledge of the functional role of miR-145 in therapeutic resistance and the tumor microenvironment. It may serve as an innovative biomarker for therapeutic response and cancer prognosis.

Keywords: MiR-145; Therapeutic sensitivity; biomarker; cancer; therapeutic resistance.

© 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

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Conflict of interest statement

The authors have no conflict of interest.

Figures

FIGURE 1

FIGURE 1

Venn diagram of potential targets of miR‐145 by bioinformatics

FIGURE 2

FIGURE 2

Regulatory mechanisms of miR‐145 in cancer therapy resistance by increasing drug efflux. MiR‐145 was sponged by circPVT1, lncRNA CACS15, LINC00707 and lncRNA HOTAIR, which blocked the downstream PI3K/AKT signaling or target genes, thus directly or indirectly inhibiting P‐gp, MRP1 and BCRP

FIGURE 3

FIGURE 3

Regulatory mechanisms of miR‐145 in cancer therapy resistance by inhibiting cancer stem cells (CSC) properties. MiR‐145 was sponged by lncRNA‐LET, lncRNA MALAT1 and lncRNA ROR, and concomitantly suppressed CD44, SOX2, KLF4, HMGA2, OCT4 and Nanog

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