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Updated: Jan 29, 2026

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption
Published on: October 4, 2019
Suppression of connexin 43 expression by miR-106a promotes melanoma cell proliferation
1Department of Burn and Plastic Surgery, Cangzhou Central Hospital, Cangzhou City, Hebei Province, China. wangjunling1994@yeah.net.
Objective:
Connexin 43 (Cx43), a vital gap junction protein is reported to be involved in melanoma progression. The aim of the study is to investigate the regulatory role of Cx43 in melanoma.
Materials And Methods:
Western blot assay was used to detect the protein expression of Cx43 in melanoma cells and the human epidermal melanocytes (HEMn). MTT cell proliferation and cell colony formation assays were used to assess cell proliferation. Bioinformatics prediction, luciferase reporter assay, Western blot and qRT-PCR assays were applied to demonstrate that Cx43 was a direct target of miR-106a in melanoma cells.
Results:
Connexin 43 (Cx43) was lower expressed in melanoma cells compared with human epidermal melanocytes (HEMn). Cx43 overexpression significantly inhibited melanoma cell proliferation and colony formation ability in vitro. However, knockdown of Cx43 had opposite effects on cell proliferation and colony formation. Bioinformatics prediction and luciferase reporter assays demonstrated that miR-106a targeted the 3' untranslated region (3'UTR) of Cx43 and regulated its mRNA and protein expression levels in melanoma cells. MiR-106a was upregulated in melanoma cells, and its overexpression attenuated the effects caused by upregulating Cx43 expression.
Conclusions:
Thus, our results indicated that Cx43 was downregulated in melanoma cells and may be a potential target of melanoma treatment.
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