PLCD1 (Phospholipase C Delta 1)

These data suggested that the effects of PLCδ1 reduction were due to a PIP2 increase and that the plasma membrane PIP2 levels affected integrin conformation in the absence of ligands. Our results revealed that PLCδ1 finely tunes integrin-mediated cell adhesion and migration and integrin conformation by altering available PIP2 levels in the plasma membrane.

PLCD1 functions as a tumor suppressor in HGSOC and is associated with improved clinical outcomes. These findings suggest that PLCD1 may serve as a prognostic biomarker and potential therapeutic target in ovarian cancer.

Through gene ontology enrichment analysis, we identify known pathways involved in melanoma, actinic keratoses, and squamous cell carcinoma and uncover additional pathways. We also uncover 5 protein-coding variants, which, to our knowledge, have not been previously reported, including LRP3 for lipomas, PLCD1 for sebaceous cysts, EIF3CL for lichen planus, TTK for pilonidal cysts, and MAPK15 for systemic lupus erythematosus.

Hence, our findings suggest novel mechanisms that affect the occurrence of GBM development, growth, and/or establishment and may also serve as secretory biomarkers for GBM prognosis and possible targets for therapy. So, continued research in this field may uncover new avenues for therapeutic interventions and contribute to the ongoing efforts to combat GBM effectively.

MicroRNA-191 regulates oral squamous cell carcinoma cells growth by targeting PLCD1 via the Wnt/β-catenin signaling pathway. Thus, miR-191 may serve as a potential target for the treatment of OSCC.

Our results demonstrate that PLCD1 is a potent tumor suppressor frequently inactivated by promoter methylation in RCC and exerts its tumor suppressive functions via suppressing WNT/β-catenin and EGFR-FAK-ERK signaling. These findings establish PLCD1 as a promising prognostic biomarker and treatment target for RCC.

Moreover, KIF14 was extensively considered as an involved tumor-promoting gene that could be affected by miR-17-3p/PLCD1 axis based on BioGRID analysis and CO-IP assay. Concludingly, this study exhibited that miR-17-3p facilitated CC progression by PLCD1 downregulation.

Overexpressed PLCD1-induced DNA damage caused cell cycle blocking and apoptosis in vitro and in vivo. PLCD1 could be a novel target in high-grade chondrosarcoma for further drug development.

However, in the presence of both ORC1 and PLCD1 overexpression, the suppressive effects of PLCD1 overexpression alone on cell proliferation, invasion, migration and EMT were attenuated. In conclusion, ORC1 was indicated to inhibit PLCD1, thus regulating the proliferation, migration and EMT processes of lung adenocarcinoma cells, which suggested that ORC1 might be a target for the treatment of lung adenocarcinoma.

Clinically, NSCLC patients with low circ-PLCD1 expression had larger tumor size, later clinical stage and shorter survival time than those with high circ-PLCD1 expression. Altogether, our findings reveal the important tumor suppressive role of circ-PLCD1 in NSCLC, reactivation of this circRNA may be considered as a novel therapeutic avenue for patient with NSCLC.

Our results demonstrated that both anti-PtdIns(4,5)P2 and anti-PtdIns(3,4,5)P3 antibodies were localized everywhere in cell. Our results suggest that PLCδ1-PH-GFP and Btk-PH-GFP/mCherry have more specificity, reliability, suitability and accuracy than antibodies in binding with and detecting PtdIns(4,5)P2 and PtdIns(3,4,5)P3 and in studying the molecular dynamics of phospholipids in live and fixed cells.

The results of double luciferase reporter gene assay showed that PLCD1 gene was a target gene of miRNA-191. miRNA-191 promote the proliferation, migration and invasion of prostate cancer PC-3 cells by targeting PLCD1.