Abstract

In this short report, we pinpoint some technical and conceptual flaws that we found in the article entitled “miR-204-5p and miR-211-5p contribute to BRAF inhibitor resistance in melanoma” (Díaz-Martínez et al., Cancer Research 2018). We also discuss how, in our opinion, these flaws led Díaz-Martínez and colleagues to incorrect conclusions about the biological role that miR-204 and miR-211 play in melanoma and about the terms of their involvement in the phenomenon of resistance to BRAF inhibitors.

Highlights

  • It is unclear why the authors discarded miR504 due to its low expression levels and yet they went after miR-211 that is expressed even less (Figure 1)

  • We and others have extensively demonstrated both in vitro and using patient data that miR-204 rather exerts its activity in sensitive cells, where its induction upon vemurafenib treatment is very robust, it targets AP1S2 and it potentiates the anti-motility effects of the drug, in turn behaving as an oncosuppressor [2, 5]

  • The location of the primers used for the qRT-PCR detection of TRPM1 host gene is suboptimal (Figure 2). miR-204 is likely detected instead of or together with miR-211 and this is why they both show a ~2-fold increase in expression according to qRT-PCR

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Summary

Introduction

It is unclear why the authors discarded miR504 due to its low expression levels and yet they went after miR-211 that is expressed even less (Figure 1). MiR-204 was chosen because its levels are ~2fold higher in A375-VR vs A375, as detected by small RNA-seq and confirmed by qRT-PCR. This claim is formally supported only by the mild decrease in proliferation that A375-VR show when transfected with a miR-204 inhibitor and exposed to vemurafenib (Figure 5E in reference 1) [3,4].

Results
Conclusion

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