Previous studies have shown the potent anti-tumor effect of paeonol, a natural compound extracted from traditional Chinese herb medicine. However, the therapeutic effect and underlying mechanisms of paeonol in melanoma are largely unknown. Two melanoma cell lines (M14 and A375) were cultured in the presence of paeonol. Cell proliferation was determined by colony formation and cell-counting kit 8 assays. Real-time quantitative reverse transcription polymerase chain reaction and Western blot were performed to detect mRNA and protein expression, respectively. Paeonol treatment significantly inhibited the colony formation and proliferation of melanoma cells by enhancing the expression of the well-characterized tumor suppressor microRNA (miR)-143. Block of miR-143 diminished the inhibitory effects of paeonol on cell growth. miR-143 directly bound to Wnt family member 5B (WNT5B) gene. Paeonol therefore down-regulated WNT5B expression through miR-143. Moreover, paeonol suppressed melanoma growth in vivo. Our study reveals that paeonol effectively suppresses melanoma cell growth both in vitro and in vivo through miR-143/WNT5B axis, which shows potential for the treatment of melanoma.
C‐MYC‐mediated keloid fibroblasts proliferation and collagen deposit may contribute to the development of keloids. F‐box and leucine‐rich repeat protein 6 (FBXL6) is reported to be involved in tumour progression, while the role of FBXL6 in keloid fibroblasts is not deciphered. Normal control skins, hypertrophic scars and keloid tissues were collected and prepared for FBXL6 detection. FBXL6 short hairpin RNAs (shRNAs) or FBXL6 over‐expression plasmids were transfected into keloid fibroblasts, and then c‐MYC plasmids were further transfected. Cell viability was assayed with a Cell‐Counting Kit‐8 kit. The relative expression of FBXL6, Cyclin A1, Cyclin D2, Cyclin E1 and Collagen I was detected with real‐time PCR and Western blot. Elevated FBXL6 expression could be observed in keloid tissues and hypertrophic scars. FBXL6 shRNAs transfection could inhibit the viability of keloid fibroblasts with diminished c‐MYC expression and down‐regulated Cyclin A1, Cyclin D2, Cyclin E1 and Collagen I expression. At the same time, overexpressed FBXL6 could promote the proliferation of keloid fibroblasts. Overexpression of c‐MYC could promote the proliferation of keloid fibroblasts reduced by FBXL6 shRNAs with up‐regulated Cyclin A1 and Collagen I expression. FBXL6 could promote the growth of keloid fibroblasts by inducing c‐MYC expression, which could be targeted in keloids treatment.
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