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Human Melanoma Cells Differentially Express RNASEL/RNase-L and miR-146a-5p under Sex Hormonal Stimulation.
Elisa Orlandi1, Elisa De Tomi1, Rachele Campagnari2
1Section of Biology and Genetics, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Strada Le Grazie, 8, 37134 Verona, Italy.
Current Issues in Molecular Biology
|October 26, 2022
Summary
Sex hormones influence melanoma progression. Testosterone increases miR-146a and decreases RNase-L, while 17β-estradiol increases RNASEL, potentially worsening outcomes in male melanoma patients.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Polymorphisms in RNASEL and miR-146a are linked to sex-specific melanoma outcomes.
- Sex hormones may mediate observed sex differences in melanoma incidence and survival.
Purpose of the Study:
- To investigate the effects of testosterone and 17β-estradiol on RNASEL and miR-146a expression in melanoma cells.
- To elucidate the role of miR-146a as a direct target of RNASEL.
Main Methods:
- Utilized luciferase reporter assays to confirm direct targeting of RNASEL by miR-146a.
- Employed qPCR and Western blot analyses to assess gene and protein expression.
- Investigated hormone effects on endogenous RNASEL and miR-146a levels in melanoma cell lines.
Main Results:
- miR-146a directly targets RNASEL in melanoma cells.
- miR-146a overexpression repressed RNase-L protein levels and increased ERK1/2 activation, indicating a pro-tumorigenic role.
- Testosterone increased miR-146a expression and decreased RNase-L protein.
- 17β-estradiol enhanced RNASEL mRNA levels and increased RNase-L protein expression.
Conclusions:
- Testosterone's pro-tumor activity in melanoma may be enhanced by miR-146a upregulation and RNase-L downregulation.
- Hormonal regulation of RNASEL and miR-146a contributes to sex-specific melanoma progression.
- Findings suggest mechanisms underlying worse outcomes in male melanoma patients.
