ArticleScientific reports2026
ADAM15 promotes the progression and metastasis of hepatocellular carcinoma by activating the JNK/p38 pathway.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
ADAM15, as a member of the membrane-bound protease family, participates prominently in the progression and metastasis of various tumours. However, its mechanism of action in hepatocellular carcinoma remains unclear. The functional role of ADAM15 in hepatocellular carcinoma (HCC) was investigated both in vitro and in vivo. ADAM15 knockdown inhibited the proliferation, migration and invasion of HCC cells, whereas ADAM15 overexpression enhanced these malignant behaviors. The results of apoptosis assay showed that inhibition of ADAM15 expression promoted apoptosis of HCC cells, and overexpression of ADAM15 inhibited apoptosis of HCC cells. Western Blot results showed that ADAM15 knockdown inhibited EMT transition and decreased the expression of mesenchymal marker N-cadherin. Additionally, ADAM15 silencing increased the expression of the pro-apoptotic protein Bax while decreasing the anti-apoptotic protein Bcl-2. The results of subcutaneous tumor formation assay in nude mice showed that knockdown of ADAM15 expression significantly inhibited the growth of subcutaneous tumors. The results of tail vein lung metastasis assay showed that ADAM15 knockdown inhibited lung metastasis of hepatocellular carcinoma in nude mice. In the mechanistic study, overexpression of ADAM15 activated the JNK-p38MAPK pathway, thereby promoting EMT and suppressing apoptosis in HCC cells. Conversely, ADAM15 knockdown inhibited the JNK-p38 MAPK pathway, leading to enhanced apoptosis and suppressed EMT. ADAM15 is highly expressed in hepatocellular carcinoma. ADAM15 regulates the apoptosis and EMT of hepatocellular carcinoma cells by activating the JNK-p38 MAPK signaling pathway, thereby promoting the progression and metastasis of hepatocellular carcinoma.
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