Panoply™ Human IL23A Over-expressing Stable Cell Line

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths worldwide, with metastasis and recurrence posing significant clinical challenges. Although the pro-inflammatory cytokine interleukin-23 (IL-23) has been linked to tumor progression, its cell-autonomous functions within HCC tumor cells remain unclear. Here, researchers found that IL-23 is significantly upregulated in HCC tumor tissues, with even higher expression levels observed in metastatic lesions. Knockdown of the IL-23 receptor (IL-23R) inhibited HCC cell proliferation, colony formation, and migration, whereas overexpression of endogenous IL-23 enhanced these phenotypes. Transcriptomic analysis revealed the enrichment of multiple oncogenic signaling pathways, including TGF-β, JAK/STAT, Hippo, MAPK, and PI3K/AKT/mTOR. Mechanistic studies demonstrated that IL-23 overexpression upregulated the expression of EGFR, AKT, and p-AKT, thereby establishing a novel IL-23/EGFR/AKT signaling axis that drives malignant phenotypes. These findings indicate that autocrine IL-23 promotes HCC progression by enhancing cell proliferation and metastatic potential through the activation of various oncogenic pathways, particularly the autocrine IL-23/EGFR/AKT axis.

In this study, the researchers generated IL-23-overexpressing HCCLM3 and Huh7 cell lines. qRT-PCR and Western blot analyses confirmed that the mRNA and protein levels of IL-23p19 and IL-23p40 were significantly elevated in IL-23-overexpressing HCCLM3 and Huh7 cells compared to their respective controls (Figure 1A–C). Furthermore, ELISA was used to measure IL-23 concentrations in the culture supernatants of the HCC cells. The results demonstrated a significant increase in IL-23 secretion by the IL-23-overexpressing cells, validating the efficacy of the strategy to enhance IL-23 production in HCC cells (Figure 1D). Over a 72-hour observation period, the IL-23-overexpressing cells exhibited significantly accelerated proliferation rates compared to their respective control cells (Figure 1E). Representative images and quantitative analysis from wound-healing assays revealed that high IL-23 expression significantly enhanced cell migration (Figure 1F and G). Colony formation assays showed that the number of colonies formed by IL-23-overexpressing cells was significantly higher than that of the respective control groups (Figure 1H and I). These results indicate that high endogenous IL-23 expression promotes cell proliferation, colony formation, and motility via autocrine signaling pathways, thereby enhancing the malignant phenotype of HCC cells.

Figure 1. Endogenous IL-23 overexpression enhances HCC cell proliferation and migration. (Zhou X, et al., 2026)