Protein Kinase D3 Promotes the Reconstruction of OSCC Immune Escape Niche Via Regulating MHC-I and Immune Inhibit Molecules Expression.

Protein kinase D3 (PKD3) has been involved in various aspects of tumorigenesis and progression in many kinds of cancer types. However, whether PKD3 regulates immune escape in tumor microenvironment is rarely reported. Here, we explored the function and mechanism of PKD3 in reconstructing the immune escape niche of oral squamous cell carcinoma (OSCC).

Protein kinase D1 induced epithelial-mesenchymal transition and invasion in salivary adenoid cystic carcinoma via E-cadherin/Snail regulation.

Salivary adenoid cystic carcinoma (SACC) is a malignant tumor, which is characterized by a higher incidence of distant metastasis. The aim of this study was to investigate the role and mechanism of protein kinase D1 (PKD1) in regulating the epithelial-mesenchymal transition (EMT) and promotes the metastasis in SACC. We analyzed the expression of PKD1 in 40 SACC patients and different metastatic potential cell lines.

Small-Molecule Inhibitor Targeting Protein Kinase D: A Potential Therapeutic Strategy.

The protein kinase D (PKD) family is a family of serine-threonine kinases that are members of the calcium/calmodulin-dependent kinase (CaMK) superfamily. PKDs have been increasingly implicated in multiple pivotal cellular processes and pathological conditions. PKD dysregulation is associated with several diseases, including cancer, inflammation, and obesity.

Salivary KLK5 and uPA are potential biomarkers for malignant transformation of OLK and OLP.

Background: Oral squamous cell carcinoma (OSCC) usually originates from oral potentially malignant disorders (OPMD), such as oral leukoplakia (OLK) and oral lichen planus (OLP). Identifying biomarkers for the early diagnosis and evaluation of malignant transformation in OPMD could improve the survival rate of OSCC patients.

Objective: The present study aimed to screen for potential salivary biomarkers for evaluating the malignant transformation of OPMD.

PKD3 promotes metastasis and growth of oral squamous cell carcinoma through positive feedback regulation with PD-L1 and activation of ERK-STAT1/3-EMT signalling.

Oral squamous cell carcinoma (OSCC) has a high incidence of metastasis. Tumour immunotherapy targeting PD-L1 or PD-1 has been revolutionary; however, only a few patients with OSCC respond to this treatment. Therefore, it is essential to gain insights into the molecular mechanisms underlying the growth and metastasis of OSCC.

[Expression Level of Protein Kinase D in Oral Squamous Cell Carcinoma with Diverse Differentiation].

Objective: This study aimed to investigate the expression level of protein kinase D (PKD) in oral squamous cell carcinoma (OSCC) and its relationship with differentiation of OSCC.

Methods: Sample was collected from 10 healthy control subjects and 40 OSCC confirmed by histopathological diagnosis, and the immunohistochemical staining was adopted to detect the expression of PKDs in OSCC tissues. The proportion of stained cell and staining intensity were evaluated to get a score, which used to analyze the difference among PKD1, PKD2 and PKD3 in various differentiation OSCC tissues.

Protein kinase D3 regulates the expression of the immunosuppressive protein, PD‑L1, through STAT1/STAT3 signaling.

Oral squamous cell carcinoma (OSCC) is capable of constructing a favorable immune escape environment through interactions of cells with cells and of cells with the environment. Programmed death ligand‑1 (PD‑L1) is a well‑recognized inhibitor of anti‑tumor immunity that plays an important role in tumor immune escape. However, the molecular mechanisms regulating PD‑L1 expression are not yet fully understood.

[Research progression of the relationship between integrin α2β1 and drug-induced gingival overgrowth].

Drug-induced gingival overgrowth (DIGO) is characterized by fibrous gingival hyperplasia and increased gingival volume. DIGO is histologically associated with proliferation of cells and deposition of extracellular matrices, particularly collagen. Integrin α2β1 is related to collagen phagocytosis and involved in the occurrence and progression of DIGO.