Meox1 silencing inhibits hepatocellular carcinoma cell proliferation, migration, and invasion by reducing G1-phase cells and p21 expression

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, characterized by high recurrence rates and limited effective therapeutic options, especially in advanced stages. Current treatments often face challenges due to tumor heterogeneity and drug resistance, necessitating the identification of novel molecular targets. The homeobox gene Meox1 (mesenchyme homeobox 1) is known to be aberrantly expressed in various malignancies, suggesting a potential role in cancer progression. However, its specific involvement and underlying mechanisms in HCC pathogenesis have remained largely unexplored, representing a critical knowledge gap.

This in vitro study investigated the role of Meox1 in HCC using human HCC cell lines (e.g., Hep G2 cells, as indicated by MeSH terms). Researchers employed Meox1 silencing as the intervention to assess its impact on cellular functions. Cell proliferation was quantified using CCK-8 assays, while clonogenic capacity was determined via clonogenic assays. Cell migration and invasion capabilities were evaluated using Transwell assays. Cell cycle distribution was analyzed by flow cytometry, and the expression of key proteins, including p21CIP1/WAF1, was examined through Western blotting. The study compared Meox1-silenced cells against appropriate control groups (e.g., scramble siRNA-treated cells).

Meox1 silencing consistently demonstrated a significant inhibitory effect across multiple HCC cell functions. Specifically, Meox1 knockdown significantly inhibited cell proliferation and clonogenic capacity, indicating a crucial role for Meox1 in sustaining HCC growth. Furthermore, Meox1 suppression significantly reduced the migratory and invasive potential of HCC cells, suggesting its involvement in metastatic processes. Cell cycle analysis revealed a distinct alteration in cell cycle progression:

Meox1 knockdown led to a reduction in G1-phase cells with a marked accumulation in the G2 phase, implying a cell cycle arrest or delay at the G2/M checkpoint. Western blot analysis provided mechanistic insights, showing that the suppression of Meox1 expression resulted in a reduced expression of p21CIP1/WAF1. While the abstract reports these effects as 'significant', specific quantitative data such as percentages, fold-changes, or p-values were not provided, limiting the precise magnitude of the observed changes.