Indirubin treatment was associated with modulation of the PI3K/AKT and MAPK pathways and induction of apoptosis and autophagy

Cancer research · Cervical cancer

Indirubin treatment was associated with modulation of the PI3K/AKT and MAPK pathways and induction of apoptosis and autophagy

This study investigated the effects of indirubin on autophagy and apoptosis in cervical cancer models, with a focus on elucidating the underlying molecular mechanisms. A xenograft tumor model in BALB/c-Nude mice and in vitro experiments using HeLa cell lines were employed. Indirubin treatment demonstrated a concentration-dependent inhibition of cervical cancer cell growth, accompanied by the induction of apoptosis and autophagy. Mechanistic analysis revealed that these effects were associated with the modulation of the PI3K/AKT signaling axis. This was evidenced by enhanced autophagic flux, indicated by an increased LC3-II/LC3-I ratio and decreased P62 expression, and concurrent induction of mitochondrial apoptosis, marked by upregulated pro-apoptotic Bax and downregulated anti-apoptotic Bcl-2 levels. Furthermore, indirubin treatment was linked to the inhibition of the MEKK1/SEK1/JNK/AP-1 signaling pathway, which may also contribute to its anti‑tumor effects. These findings suggest that the anti‑tumor activity of indirubin is associated with the regulation of the PI3K/AKT and MAPK pathways, the enhancement of autophagy, and the promotion of apoptosis, providing a theoretical basis for its therapeutic potential in cervical cancer treatment.

The results provide evidence that indirubin can inhibit cervical cancer cell proliferation, promote apoptosis, and induce autophagy through the PI3K/AKT and MAPK signaling pathways, suggesting its potential as a therapeutic agent for cervical cancer.

Evidence level: Korai humán adat. Kis vagy feltáró emberi adat.

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