Variation of adhesion capability of K-ras transformed malignant cells and clinical implications

Abstract

Objective: To investigate the mechanism of carcinogenesis, invasion and metastasis. Methods: The expressions of adhesive molecule and adhesive structure in v-k-ras transformed normal rat kidney cells (KNRK) were detected with a variety of molecular biological techniques, including cell culture, immunofluorescence labeling, electron microscopy, polyacrylamide gel electrophoresis, and protein blotting, and compared with normal rat kidney (NRK) cells. Results: The significantly shortened doubling time, remarkably active proliferation ability in soft agar, and invasive growth in the abdomen of nude rat, demonstrated the malignant biological behaviors of KNRK cells. In KNRK cells, the adhesive molecules, P-cadherin, ct and 1~ catenin, actin, and adhesive structures, the adhesive junction and gap junction, were all abnormally expressed. And cell aggregation was significantly decreased. The aggregation ability disappeared at 20°C, and became active with a suitable amount of calcium solution. Conclusion: Following the transfection of virus K-ras gene, normal cells were transformed into malignant cells. In early stage of cancer, the variation of adhesive ability may be one of the vital factors underlying tumorigenesis, invasion and metastasis.

PARP-1: a critical regulator in radioprotection and radiotherapy-mechanisms, challenges, and therapeutic opportunities

“…3-AB can promote apoptotic death in HeLa cells by interfering with PARP expression and blocking G2 phase arrest following X-ray irradiation ( Masutani et al, 1995 ). Pairing the PARP inhibitor Veliparib with ionizing radiation can swiftly trigger senescence in tumor cells ( Zhang et al, 2016 ). The PARP-1 inhibitor amplifies ionizing radiation-induced cytotoxicity by suppressing NF-κB activation ( Veuger et al, 2009 ).…”