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Relationship between IL10 and PD-L1 in Liver Hepatocellular Carcinoma Tissue and Cell Lines
Qian Qian1, Changping Wu1, Jianping Chen1
1Department of Tumor Biological Treatment, Department of Oncology, The Third Affiliated Hospital of Soochow University, 185 Juqian Street, 213003, China.
Background:
Despite the large-scale clinical application of programmed death-ligand 1 (PD-L1) monoclonal antibody, reduction in its clinical response rate has become a gradual problem. As such, use of PD-L1 monoclonal antibody in combination with other anticarcinoma drugs has been the main strategy in improving its efficacy. Interleukin 10 (IL10) is a recognized inflammatory and immunosuppressive factor. Previous studies have suggested that there is a link between PD-L1 and IL10.
Objective:
This study was aimed at clarifying the relationship between PD-L1 and IL10 in liver hepatocellular carcinoma (LIHC) and whether IL10 enhances the efficacy of PD-L1 inhibitor.
Methods:
Expression levels of PD-L1 and IL10 in carcinoma and adjacent tissues were tested by immunochemistry, Western blotting, and RT-PCR. Survival duration and follow-up data of each patient were recorded. LIHC cell lines Bel7405 and MHCC 97-H were used for in vitro experiments. Exogenous IL10 and anti-IL10 were added to cell supernatant. Expression level of PD-L1 in the LIHC cell lines was determined using Western blotting and ELISA. CCK8 and transwell assays were adopted to examine the effect of PD-L1 combined with IL10 on proliferation, invasion, and metastasis of LIHC cells.
Results:
The survival period of patients with low expression of IL10 was longer than that of patients with high expression (P = 0.01). Overexpression of PD-L1 increased the IL10 and Met levels in LIHC tissues and cell lines. IL10 downregulated the expression level of PD-L1 and enhanced the efficacy of crizotinib via the Met signaling pathway in the LIHC cells.
Conclusions:
A combination of IL10 and PD-L1 inhibitor holds great promise as an effective treatment for LIHC.
Insights
Interleukin 10 (IL10) can enhance the efficacy of programmed death-ligand 1 (PD-L1) inhibitors in liver cancer. This study found IL10 downregulates PD-L1, improving treatment outcomes for liver hepatocellular carcinoma (LIHC).
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Programmed death-ligand 1 (PD-L1) inhibitors show reduced efficacy over time.
- Combining PD-L1 inhibitors with other drugs is a strategy to improve outcomes.
- Interleukin 10 (IL10) is an immunosuppressive factor linked to PD-L1.
Purpose of the Study:
- To clarify the relationship between PD-L1 and IL10 in liver hepatocellular carcinoma (LIHC).
- To determine if IL10 enhances the efficacy of PD-L1 inhibitors in LIHC.
Main Methods:
- Immunohistochemistry, Western blotting, and RT-PCR were used to assess PD-L1 and IL10 expression in LIHC tissues and cell lines.
- In vitro experiments involved adding IL10 or anti-IL10 to cell cultures.
- CCK8 and transwell assays evaluated the combined effects on cell proliferation and invasion.
Main Results:
- Low IL10 expression correlated with longer patient survival.
- PD-L1 overexpression increased IL10 and Met levels in LIHC.
- IL10 downregulated PD-L1 expression and enhanced crizotinib efficacy via the Met pathway.
Conclusions:
- IL10 plays a role in regulating PD-L1 expression in LIHC.
- Combined IL10 and PD-L1 inhibition shows potential for treating LIHC.
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