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7.4
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Cancers
Special Issues
miRNA Therapeutics Against Cancer
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miRNA Therapeutics Against Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (31 October 2020) | Viewed by 3398

Special Issue Editor

Prof. Dr. Yukihiro Akao

E-Mail Website
Guest Editor
United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan
Interests: roles of microRNAs in carcinogenesis; anti-cancer effect of phytochemicals; anti-cancer effect of fatty acid-analogues

Special Issue Information

Dear Colleagues,

Molecular target drugs against cancer induce tolerance by activating the alternative signal transduction pathways and developing genetic aberrations. MicroRNA (miRNA) is a group of small non-coding RNA that regulates gene expression at the translation step. MicroRNA targets every gene and depresses the growth-related signal pathways by silencing plural key genes involved in the signal pathways and systems. Accumulating evidence shows that dysregulated expression of tumor-suppressor (TS) miRNA contributes to carcinogenesis. The replacement of TS miRNA into cancer cells is a promising therapeutic because of its effect on tumor cell-specific and fewer resulting occurrences of tolerance. We will welcome papers discussing issues from miRNA medicine.

Prof. Dr. Yukihiro Akao
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • microRNA
  • tumor-suppressor
  • signal transduction pathway
  • replacement therapy
  • drug delivery system
  • drug tolerance

Published Papers (1 paper)

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Research

17 pages, 3372 KiB  
Article
Synthetic MIR143-3p Suppresses Cell Growth in Rhabdomyosarcoma Cells by Interrupting RAS Pathways Including PAX3–FOXO1
by Nobuhiko Sugito, Kazuki Heishima, Yuko Ito and Yukihiro Akao
Cancers 2020, 12(11), 3312; https://doi.org/10.3390/cancers12113312 - 10 Nov 2020
Cited by 5 | Viewed by 3022
Abstract
Rhabdomyosarcoma (RMS) is a soft tissue sarcoma most frequently found in children. In RMS, there are two major subtypes, embryonal RMS (ERMS) and alveolar RMS (ARMS). ARMS has the worse prognosis of the two owing to the formation of the chimeric PAX3–FOXO1 gene. [...] Read more.
Rhabdomyosarcoma (RMS) is a soft tissue sarcoma most frequently found in children. In RMS, there are two major subtypes, embryonal RMS (ERMS) and alveolar RMS (ARMS). ARMS has the worse prognosis of the two owing to the formation of the chimeric PAX3–FOXO1 gene. A novel therapeutic method is required for treating ARMS. In our previous study, we found that the ectopic expression of chemically modified MIR143-3p#12 (CM-MIR143#12), which is RNase-resistant and shows the highest anti-proliferation activity among the synthesized MIR143 derivatives that were tested, induces significant cell growth suppression by targeting KRAS, AKT, and ERK in colorectal cancer cells. The expression of MIR143-3p in RMS was dramatically downregulated compared with that of normal tissue. Ectopic expression of CM-MIR143#12 in RMS cells resulted in a significant growth inhibitory effect through the induction of apoptosis and autophagy. Interestingly, we found that CM-MIR143#12 also silenced the expression of chimeric PAX3–FOXO1 directly and, using siR-KRAS or siR-AKT, that KRAS networks regulated the expression of PAX3–FOXO1 in ARMS cells. In ERMS harboring NRAS mutation, CM-MIR143#12 silenced mutated NRAS. These findings indicate that CM-MIR143#12 efficiently perturbed the RAS signaling pathway, including the ARMS-specific KRAS/PAX3–FOXO1 networks. Full article
(This article belongs to the Special Issue miRNA Therapeutics Against Cancer)
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