2. Academic Validation
  3. Serine/Threonine Kinase (STK) 33 promotes the proliferation and metastasis of human esophageal squamous cell carcinoma via inflammation-related pathway

Serine/Threonine Kinase (STK) 33 promotes the proliferation and metastasis of human esophageal squamous cell carcinoma via inflammation-related pathway

  • Pathol Res Pract. 2024 Feb:254:155154. doi: 10.1016/j.prp.2024.155154.
Haifeng Jiang 1,  Liping Li 2,  Tao Ma 1,  Ruixiao Wang 1,  Xiaozhen Chen 1,  Ke Xu 3,  Chen Chen 4,  Zijin Liu 5,  Hongmei Wang 6,  Lingyan Huang 7
Affiliations

Affiliations

  • 1 Department of Pathology, General Hospital of Ningxia Medical University, Yinchuan 750004, China.
  • 2 Public Health and Management College in Ningxia Medical University, Yinchuan 750004, China.
  • 3 Department of Pathology, General Hospital of Ningxia Medical University, Yinchuan 750004, China; Ningxia Armed Police Corps, Yinchuan 750004, China.
  • 4 Department of Otolaryngology-Head and Neck Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China; Department of Pathology and Pathophysiology, Shandong University, Cheeloo Healthy Science Center, Jinan 250012, China.
  • 5 Clinical Medical College in Ningxia Medical University, Yinchuan 750004, China.
  • 6 Department of Pharmacology, School of Medicine, Southeast University, Nanjing 210009, Jiangsu, China; School of Medicine, Shanxi University of Chinese Medicine, Xi'an 712046, China. Electronic address: 101012573@seu.edu.cn.
  • 7 Department of Pathology, General Hospital of Ningxia Medical University, Yinchuan 750004, China. Electronic address: kaixinhly@126.com.
PMID: 38286054 DOI: 10.1016/j.prp.2024.155154
Abstract

The serine/threonine kinase (STK) 33 plays a key role in Cancer cell proliferation and metastasis. Abnormal STK33 expression is closely related to malignancy of numerous cancers. This study suggests the important role of STK33 in the pathogenesis and metastatic progression of esophageal squamous cell carcinoma (ESCC). STK33 expression in human ESCC tissues was detected by immunohistochemical technique. Further, we analyzed the relationship between STK33 and clinical and pathological factors as well as the prognosis of patients. ECa109 cell line was cultured and transfected with STK33-RNAi lentiviral vector to perform Hochest33342 & PI and metastasis experiments. The TCGA database was used to analyze the STK33 expression level in ESCC. All statistical analyses were performed in SPSS 23.0 software. Differences with P < 0.05 were considered statistically significant. In human ESCC specimens, STK33 was overexpressed and associated with poor prognosis. Silencing STK33 expression suppressed ESCC proliferation, migration, invasion, and tumor growth. STK33 also mediated angiogenesis, TGFβ, and inflammatory response in ESCC. Mechanistic investigations revealed that STK33 regulates ESCC through multiple complex pathways. Dysregulated STK33 signaling promotes ESCC growth and progression. Thus, our findings identified STK33 as a candidate treatment target that improves ESCC therapy.

Keywords

Esophageal squamous cell carcinoma; Inflammation response; Metastasis; Proliferation; STK33.

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