HSF1 is involved in immunotherapeutic response through regulating APOJ/STAT3-mediated PD-L1 expression in hepatocellular carcinoma

Cancer Biol Ther. 2023 Dec 31;24(1):1-9. doi: 10.1080/15384047.2022.2156242.

Abstract

Hepatocellular cancer (HCC) is a serious illness with high prevalence and mortality throughout the whole world. For advanced HCC, immunotherapy is somewhat impactful and encouraging. Nevertheless, a substantial proportion of patients with advanced HCC are still unable to achieve a durable response, owing to heterogeneity from clonal variability and differential expression of the PD-1/PD-L1 axis. Recently, heat shock factor 1 (HSF1) is recognized as an important component of tumor immunotherapeutic response as well as related to PD-L1 expression in cancer. However, the mechanism of HSF1 regulating PD-L1 in cancer, especially in HCC, is still not fully clear. In this study, we observed the significantly positive correlation between HSF1 expression and PD-L1 expression in HCC samples; meanwhile combination expressions of HSF1 and PD-L1 served as the signature for predicting prognosis of patients with HCC. Mechanistically, HSF1 upregulated PD-L1 expression by inducing APOJ expression and activating STAT3 signaling pathway in HCC. In addition, we explored further the potential values of targeting the HSF1-APOJ-STAT3 axis against CD8+ T cells-mediated cancer cells cytotoxicity. These findings unveiled the important involvement of HSF1 in regulating PD-L1 expression in HCC as well as provided a novel invention component for improving the clinical response rate and efficacy of PD-1/PD-L1 blockade.

Keywords: APOJ; HSF1; Hepatocellular carcinoma; JAK/STAT3; PD-L1; immunotherapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • B7-H1 Antigen / genetics
  • CD8-Positive T-Lymphocytes
  • Carcinoma, Hepatocellular* / genetics
  • Carcinoma, Hepatocellular* / therapy
  • Heat Shock Transcription Factors* / genetics
  • Humans
  • Immunotherapy*
  • Liver Neoplasms* / genetics
  • Liver Neoplasms* / therapy
  • Programmed Cell Death 1 Receptor / genetics
  • STAT3 Transcription Factor / genetics

Substances

  • B7-H1 Antigen
  • Programmed Cell Death 1 Receptor
  • STAT3 protein, human
  • STAT3 Transcription Factor
  • HSF1 protein, human
  • CLU protein, human
  • Heat Shock Transcription Factors

Grants and funding

This work was financially supported by National Natural Science Foundation of China (Grant No. 81872492) and Shanghai Natural Science Fund (Grant No. 15ZR1406300) to K.G.