AnnexinA7 down-regulation might suppress the proliferation and metastasis of human hepatocellular carcinoma cells via MAPK/ ERK pathway.

Background: Hepatocellular carcinoma is one of the most fatal malignancies worldwide with high lethality. However, the exact mechanism of liver tumorigenesis is still unclear. AnnexinA7 (ANXA7) is a Ca2+-binding protein which is involved in membrane organization and dynamics and indicated a role of ANXA7 in cancer.

Potential biomarkers of DNA replication stress in cancer.

Oncogene activation is an established driver of tumorigenesis. An apparently inevitable consequence of oncogene activation is the generation of DNA replication stress (RS), a feature common to most cancer cells. RS, in turn, is a causal factor in the development of chromosome instability (CIN), a near universal feature of solid tumors.

GALNT14 mediates tumor invasion and migration in breast cancer cell MCF-7.

Aberrant glycosylation is a hallmark of most human cancers and affects many cellular properties, including cell proliferation, apoptosis, differentiation, transformation, migration, invasion, and immune responses. Here, we report that N-acetylgalactosaminyltransferase14 (GALNT14), which mediates the initial step of mucin-type O-glycosylation and is heterogeneously expressed in most breast cancers, plays a critical role in the invasion and migration of breast cancers by regulating the activity of MMP-2 and expression of some EMT genes. We have modulated the expression of GALNT14 by RNAi and overexpression in MCF-7 cells.

Lgr5 expression as stem cell marker in human gastric gland and its relatedness with other putative cancer stem cell markers.

To explore Lgr5 as the possible stem cell marker in human gastric tissue, 259 normal gastric tissues and dissected gastric adenocarcinoma were analyzed by immunohistochemistry, immunofluorescence double staining and qRT-PCR. The results demonstrated that Lgr5 was expressed in the bottom of the normal gastric gland units, and showed a differential expression in gastric adenocarcinoma with varying differentiation. Lgr5 and Bmi1 were co-expressed within the same cells of gastric glands.

Insulin-like factor binding protein-3 promotes the G1 cell cycle arrest in several cancer cell lines.

Insulin-like growth factor binding protein-3 (IGFBP-3) is a multi-functional protein known to induce apoptosis of various cancer cells in an insulin-like growth factor (IGF)-dependent and IGF-independent manner. In our previous study, we found that IGFBP-3 induced apoptosis through the activation of caspases in 786-O cells. In this study, we further examined that whether IGFBP-3 induced apoptosis through the induction of cell cycle arrest in 786-O, A549 and MCF-7 cells.

Colocalization and identification of interaction sites between IGFBP-3 and GalNAc-T14.

GalNAc-T14 was identified as a novel IGFBP-3 binding partner in previous studies. Here, we furtherly confirmed the interaction between them by confocal microscopy, and identified the binding domain and probable interaction sites of GalNAc-T14 with IGFBP-3. The result of subcellular localization indicated that GalNAc-T14 was distributed in the cytosol, whereas IGFBP-3 existed in the cytosol and nucleolus.