STAT3 and Its Targeting Inhibitors in Oral Squamous Cell Carcinoma

Jiang, Mingjing; Li, Bo

doi:10.3390/cells11193131

Cited by 36 publications

(19 citation statements)

References 175 publications

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“… 1 , 2 Notably, the 5-year survival rate for OSCC is approximately 50%, and high mortality and recurrence rates are problems that urgently need to be solved. 3 , 4 Immune escape, a phase in the “tumor immunoediting” hypothesis, refers to tumor cells escaping recognition and attack by the body’s immune system. 5 In this phase, tumor cells can mediate immune escape mediated by a series of acquired immunophenotypes.…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of DNA key protein-FEN1 inhibits OSCC growth by affecting immunosuppressive phenotypes via IFN-γ/JAK/STAT-1

Wang

Sun

et al. 2023

Int J Oral Sci

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Oral squamous cell carcinoma (OSCC) escape from the immune system is mediated through several immunosuppressive phenotypes that are critical to the initiation and progression of tumors. As a hallmark of cancer, DNA damage repair is closely related to changes in the immunophenotypes of tumor cells. Although flap endonuclease-1 (FEN1), a pivotal DNA-related enzyme is involved in DNA base excision repair to maintain the stability of the cell genome, the correlation between FEN1 and tumor immunity has been unexplored. In the current study, by analyzing the clinicopathological characteristics of FEN1, we demonstrated that FEN1 overexpressed and that an inhibitory immune microenvironment was established in OSCC. In addition, we found that downregulating FEN1 inhibited the growth of OSCC tumors. In vitro studies provided evidence that FEN1 knockdown inhibited the biological behaviors of OSCC and caused DNA damage. Performing multiplex immunohistochemistry (mIHC), we directly observed that the acquisition of critical immunosuppressive phenotypes was correlated with the expression of FEN1. More importantly, FEN1 directly or indirectly regulated two typical immunosuppressive phenotype-related proteins human leukocyte antigen (HLA-DR) and programmed death receptor ligand 1 (PD-L1), through the interferon-gamma (IFN-γ)/janus kinase (JAK)/signal transducer and activator transcription 1 (STAT1) pathway. Our study highlights a new perspective on FEN1 action for the first time, providing theoretical evidence that it may be a potential immunotherapy target for OSCC.

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Section: Introductionmentioning

confidence: 99%

Down-regulation of DNA key protein-FEN1 inhibits OSCC growth by affecting immunosuppressive phenotypes via IFN-γ/JAK/STAT-1

Wang

Sun

et al. 2023

Int J Oral Sci

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“…Adi Binder Gallimidi et al [ 30 ] proved that oral infections cause TLR signaling, which in turn causes IL-6 production and STAT3 activation. In both clinical and experimental settings, STAT3 has a significant role as a modulator of OSCC carcinogenesis [ 76 ]. These essential effectors include cyclinD1, MMP-9, and heparinase, which promote the growth and invasion of OSCC.…”

Section: Microbiome Influences Cancer Metastasis By Regulating Matrix...mentioning

confidence: 99%

Current Understanding of Microbiomes in Cancer Metastasis

Liu

Luo

Wen

et al. 2023

Cancers

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Cancer has been the first killer that threatens people’s lives and health. Despite recent improvements in cancer treatment, metastasis continues to be the main reason for death from cancer. The functions of microbiome in cancer metastasis have been studied recently, and it is proved that microbiome can influence tumor metastasis, as well as positive or negative responses to therapy. Here, we summarize the mechanisms of microorganisms affecting cancer metastasis, which include epithelial-mesenchymal transition (EMT), immunity, fluid shear stress (FSS), and matrix metalloproteinases (MMPs). This review will not only give a further understanding of relationship between microbiome and cancer metastasis, but also provide a new perspective for the microbiome’s application in cancer metastasis prevention, early detection, and treatment.

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“…Research on specific genes plays a crucial role in the diagnosis, treatment, and prognosis of OSCC. For example, NUPR1, 38 microRNA‐485‐5p, 39 and STAT 40 are known to play an essential role in OSCC development. However, the role and underlying mechanisms of EPRS in OSCC have not been thoroughly explored.…”

Section: Discussionmentioning

confidence: 99%

Evodiamine inhibits EPRS expression to regulate glutamate metabolism and proliferation of oral squamous cell carcinoma cells

Lin,

Lv,

Ren

et al. 2024

The Kaohsiung J of Med Scie

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The effects of evodiamine (EVO) on oral squamous cell carcinoma (OSCC) are not yet understood. Based on our earlier findings, we hypothesized that evodiamine may affect OSCC cell proliferation and glutamate metabolism by modulating the expression of EPRS (glutamyl‐prolyl‐tRNA synthetase 1). From GEPIA, we obtained EPRS expression data in patients with OSCC as well as survival prognosis data. An animal model using Cal27 cells in BALB/c nude mice was established. The expression of EPRS was assessed by immunofluorescence, Western blotting, and quantitative PCR. Glutamate measurements were performed to evaluate the impact of evodiamine on glutamate metabolism of Cal27 and SAS tumor cells. transient transfection techniques were used to knock down and modulate EPRS in these cells. EPRS is expressed at higher levels in OSCC than in normal tissues, and it predicts poor prognosis in patients. In a nude mouse xenograft model, evodiamine inhibited tumor growth and the expression of EPRS. Evodiamine impacted cell proliferation, glutamine metabolism, and EPRS expression on Cal27 and SAS cell lines. In EPRS knockdown cell lines, both cell proliferation and glutamine metabolism are suppressed. EPRS's overexpression partially restores evodiamine's inhibitory effects on cell proliferation and glutamine metabolism. This study provides crucial experimental evidence supporting the potential therapeutic application of evodiamine in treating OSCC. Evodiamine exhibits promising anti‐tumor effects by targeting EPRS to regulate glutamate metabolism.

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STAT3 and Its Targeting Inhibitors in Oral Squamous Cell Carcinoma

Cited by 36 publications

References 175 publications

Down-regulation of DNA key protein-FEN1 inhibits OSCC growth by affecting immunosuppressive phenotypes via IFN-γ/JAK/STAT-1

Down-regulation of DNA key protein-FEN1 inhibits OSCC growth by affecting immunosuppressive phenotypes via IFN-γ/JAK/STAT-1

Current Understanding of Microbiomes in Cancer Metastasis

Evodiamine inhibits EPRS expression to regulate glutamate metabolism and proliferation of oral squamous cell carcinoma cells

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