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Abstract <p><i>Geodoram densiflorum</i> or pink nodding orchid grows in wet habitats in Bangladesh. Rural people traditionally use this orchid’s pseudobulbs to treat skin inflammation, tumors and carbuncles. Though a protein from these bulbs previously showed antitumor activity against Ehrlich ascites carcinoma (EAC) cells in vitro, this study focused on proving this effect in vivo in a mice model and against a human cancer cell line. GDL exhibited around 45% growth inhibition against A549 cells at a concentration of 64 µg/mL implicating a caspase-dependent pathway modulated by caspase-3, -8, and -9 inhibitors. The condensed nuclei and morphological changes of GDL-treated cells indicating apoptosis also became evident by Hoechst 33342 and FITC-annexin V/PI staining. GDL up-regulated CASP9 and p53 while down-regulating PARP, MAPK, and STAT3 gene expression, suggesting the involvement of death receptor and intrinsic mitochondrial pathways. Flow cytometry analysis revealed GDL-induced G<sub>0</sub>/G<sub>1</sub> phase cell cycle arrest. In vivo, GDL inhibited EAC cell proliferation by 48%, extending EAC-bearing mice lifespan by 37.05%, and improved hematological parameters, notably increasing red blood cell counts and hemoglobin levels to 2.41 × 10<sup>9</sup> RBC/mL and 10.27 g/dL, respectively. These findings underscore the therapeutic potential of GDL, setting the stage for further in-depth research.</p>

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Geodorum densiflorum Rhizome Lectin Induces Apoptosis in Human Lung Cancer Cells and Inhibits the Growth of Ehrlich Ascites Carcinoma Cells In Vivo in Mice

  • 期刊论文

  • 发表日期：

    2025年6月1日

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  • Mizanur R. Mamun,
  • Syed R. Kabir,
  • Imtiaj Hasan,
  • A. K. M. Asaduzzaman,
  • Mohammad T. Alam

摘要

Abstract

Geodoram densiflorum or pink nodding orchid grows in wet habitats in Bangladesh. Rural people traditionally use this orchid’s pseudobulbs to treat skin inflammation, tumors and carbuncles. Though a protein from these bulbs previously showed antitumor activity against Ehrlich ascites carcinoma (EAC) cells in vitro, this study focused on proving this effect in vivo in a mice model and against a human cancer cell line. GDL exhibited around 45% growth inhibition against A549 cells at a concentration of 64 µg/mL implicating a caspase-dependent pathway modulated by caspase-3, -8, and -9 inhibitors. The condensed nuclei and morphological changes of GDL-treated cells indicating apoptosis also became evident by Hoechst 33342 and FITC-annexin V/PI staining. GDL up-regulated CASP9 and p53 while down-regulating PARP, MAPK, and STAT3 gene expression, suggesting the involvement of death receptor and intrinsic mitochondrial pathways. Flow cytometry analysis revealed GDL-induced G0/G1 phase cell cycle arrest. In vivo, GDL inhibited EAC cell proliferation by 48%, extending EAC-bearing mice lifespan by 37.05%, and improved hematological parameters, notably increasing red blood cell counts and hemoglobin levels to 2.41 × 109 RBC/mL and 10.27 g/dL, respectively. These findings underscore the therapeutic potential of GDL, setting the stage for further in-depth research.