Resultado da pesquisa (1)
Termo utilizado na pesquisa miR-144-3p
#1 - (Online First) Mechanistic investigation of miR-144-3p in suppressing hepatocellular carcinoma progression via the NFE2L2/Nrf2 axis
Abstract in English:
Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with frequent metastasis and limited therapeutic options. MicroRNAs are important regulators of tumor progression, but the role and downstream mechanism of miR-144-3p in HCC remain incompletely defined. In this study, we investigated the antitumor activity of miR-144-3p and its relationship with the NFE2L2/Nrf2 pathway. In vitro, miR-144-3p overexpression reduced Hep3B cell viability, inhibited cell-cycle progression, promoted apoptosis, and suppressed migration and invasion. Target prediction and dual-luciferase reporter assays supported NFE2L2, which encodes Nrf2, as a direct target of miR-144-3p. Consistently, miR-144-3p reduced Nrf2 expression and downregulated downstream Nrf2-related proteins, including NQO1 and HMOX1, with effects similar to Nrf2 knockdown. Reanalysis of a publicly available single-cell RNA sequencing dataset identified an Nfe2l2-positive hepatocyte progenitor cell subpopulation enriched in HCC and associated with invasion-, metastasis-, and stemness-related activity. In vivo, intratumoral administration of miR-144-3p agomir inhibited Hep3B-derived xenograft growth, increased apoptosis, and reduced Ki67 expression. These findings suggest that miR-144-3p suppresses HCC progression, at least in part, by targeting the NFE2L2/Nrf2 pathway, providing preliminary evidence of its biological relevance in comparative oncology and veterinary biomedical research
Abstract in Portuguese:
Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with frequent metastasis and limited therapeutic options. MicroRNAs are important regulators of tumor progression, but the role and downstream mechanism of miR-144-3p in HCC remain incompletely defined. In this study, we investigated the antitumor activity of miR-144-3p and its relationship with the NFE2L2/Nrf2 pathway. In vitro, miR-144-3p overexpression reduced Hep3B cell viability, inhibited cell-cycle progression, promoted apoptosis, and suppressed migration and invasion. Target prediction and dual-luciferase reporter assays supported NFE2L2, which encodes Nrf2, as a direct target of miR-144-3p. Consistently, miR-144-3p reduced Nrf2 expression and downregulated downstream Nrf2-related proteins, including NQO1 and HMOX1, with effects similar to Nrf2 knockdown. Reanalysis of a publicly available single-cell RNA sequencing dataset identified an Nfe2l2-positive hepatocyte progenitor cell subpopulation enriched in HCC and associated with invasion-, metastasis-, and stemness-related activity. In vivo, intratumoral administration of miR-144-3p agomir inhibited Hep3B-derived xenograft growth, increased apoptosis, and reduced Ki67 expression. These findings suggest that miR-144-3p suppresses HCC progression, at least in part, by targeting the NFE2L2/Nrf2 pathway, providing preliminary evidence of its biological relevance in comparative oncology and veterinary biomedical research.
