We constructed XCL1-GPC3 fusion molecules as a liver cancer vaccine by linking the XCL1 chemokine to glypican-3 (GPC3), which is overexpressed in hepatocellular carcinoma (HCC).
The results of present study indicated that the successful preparation of recombinant GPC3 protein and an anti‑human GPC3 mouse mAb may be provide a basis for developments in the diagnosis and treatment of liver cancer.
Our findings demonstrate that GPC3 is a critical regulator of glucose metabolism reprogramming in LC cells, which provides a strong line of evidence for GPC3 as an important therapeutic target to normalize glucose metabolic aberrations responsible for LC progression.
Here, by linking catalytic hairpin assembly (CHA) with electrochemical biosensors through clickable nucleic acids, we develop a facile method for the detection of liver cancer related short gene MXR7.
GPC3, a liver tumor homing peptide, was coated onto the surface of apatinib-loaded NBs through biotin-avidin interactions to target liver cancer HepG2 cells.
Ki-67 staining as the criteria of the liver cancer cell proliferation index also indicated a cross correlation between liver cancer proliferation and GPC3 levels.
Using rat models of liver cancer in the current study, we utilized nested PCR to detect Gpc3 and Afp mRNA to determine their relationship with liver cancer micrometastases.
Mutations of the GPC3 gene are responsible for Simpson-Golabi-Behmel syndrome, which is characterized by anomalies of postnatal overgrowth and an increased risk of developing pediatric malignancies, mostly Wilms tumor and liver cancer.
Flow cytometry indicated that GPC3 was highly expressed in liver CD90(+)CSCs and mature cancer cells in liver cancer cell lines and human liver tumor tissues.