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<p>Bladder cancer is one of the most prevalent cancers worldwide. Lapachol is a natural compound with antiproliferative effects, but its activity in bladder cancer cells has not yet been evaluated. Cytotoxic activity was assessed using the MTT assay, while long-term effects were evaluated through the clonogenic assay. Cell migration was assessed by the scratch assay, and cell cycle progression was analyzed via flow cytometry. The expression of the JHDM1D gene and the long non-coding RNAs (lncRNAs) JHDM1D-AS1, SBF2-AS1, and RP11-36E7.4 was investigated. Treatment resulted in a dose- and time-dependent inhibition of cell viability, accompanied by a significant reduction in clonogenic survival in all cell lines. Lapachol impaired cell migration, with RT4 cells showing the greatest sensitivity. Cell cycle analysis revealed a significant increase in the sub-G1 cell population, indicative of apoptosis, and a concomitant decrease in the G0/G1 phase. Molecular analysis revealed modulation of lncRNA expression in a cell-line-specific manner. In RT4 cells, there was a downregulation of SBF2-AS1 expression. In J82 cells, a decrease in JHDM1D-AS1 and an increase in RP11-36E7.4 expression were observed. These findings suggest that lapachol exerts significant antiproliferative effects on bladder cancer cells through mechanisms involving cell cycle arrest, apoptosis induction, and modulation of lncRNA expression, supporting its potential for bladder cancer treatment.</p>

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Lapachol interferes with the cell cycle and inhibits proliferation and migration of bladder tumor cells with effects on ncRNA expression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月30日

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  • Tatiane Roquete Amparo,
  • Kamila de Fátima da Anunciação,
  • Tamires Cunha Almeida,
  • Alaíde Braga de Oliveira,
  • Glenda Nicioli da Silva,
  • Geraldo Célio Brandão

摘要

Bladder cancer is one of the most prevalent cancers worldwide. Lapachol is a natural compound with antiproliferative effects, but its activity in bladder cancer cells has not yet been evaluated. Cytotoxic activity was assessed using the MTT assay, while long-term effects were evaluated through the clonogenic assay. Cell migration was assessed by the scratch assay, and cell cycle progression was analyzed via flow cytometry. The expression of the JHDM1D gene and the long non-coding RNAs (lncRNAs) JHDM1D-AS1, SBF2-AS1, and RP11-36E7.4 was investigated. Treatment resulted in a dose- and time-dependent inhibition of cell viability, accompanied by a significant reduction in clonogenic survival in all cell lines. Lapachol impaired cell migration, with RT4 cells showing the greatest sensitivity. Cell cycle analysis revealed a significant increase in the sub-G1 cell population, indicative of apoptosis, and a concomitant decrease in the G0/G1 phase. Molecular analysis revealed modulation of lncRNA expression in a cell-line-specific manner. In RT4 cells, there was a downregulation of SBF2-AS1 expression. In J82 cells, a decrease in JHDM1D-AS1 and an increase in RP11-36E7.4 expression were observed. These findings suggest that lapachol exerts significant antiproliferative effects on bladder cancer cells through mechanisms involving cell cycle arrest, apoptosis induction, and modulation of lncRNA expression, supporting its potential for bladder cancer treatment.