Breaking the symmetry of cell contractility drives tubulogenesis via CXCL1 polarization.

The intricate interplay between biomechanical and biochemical pathways in modulating morphogenesis is an interesting research topic. How biomechanical force regulates epithelial cell tubulogenesis remains poorly understood. Here, we established a model of tubulogenesis by culturing renal proximal tubular epithelial cells on a collagen gel while manipulating contractile force.

Assessment of Tilapia Skin Collagen for Biomedical Research Applications in Comparison with Mammalian Collagen.

Collagen is an important material for biomedical research, but using mammalian tissue-derived collagen carries the risk of zoonotic disease transmission. Marine organisms, such as farmed tilapia, have emerged as a safe alternative source of collagen for biomedical research. However, the tilapia collagen products for biomedical research are rare, and their biological functions remain largely unexamined.

EMI2 expression as a poor prognostic factor in patients with breast cancer.

Early mitotic inhibitor 2 (EMI2, gene symbol FBXO43), an APC/C inhibitor regulated by Plx1, is essential for cytostatic factor (CSF) activity. It belongs to subclass FBXO of the F-box proteins family. The aim of this study is to examine the clinicopathological significance of EMI2 in breast cancer.

Visfatin Mediates Malignant Behaviors through Adipose-Derived Stem Cells Intermediary in Breast Cancer.

Adipose-derived stem cells (ADSCs) have been implicated in tumor growth and metastasis in breast cancer. ADSCs exhibit tumor tropism, and are of increasing clinical relevance due to the autologous fat grafting for breast reconstruction. Although we have previously shown that a high level of the adipocytokine visfatin in human breast cancer tissues correlated with tumor progression mediated by cAbl and STAT3, the effects of visfatin in the tumor microenvironment are unclear.

. 9°N DNA polymerase exhibits 3'-esterase activity that can be harnessed for DNA sequencing.

It was reported in 1995 that T7 and Taq DNA polymerases possess 3'-esterase activity, but without follow-up studies. Here we report that the 3'-esterase activity is intrinsic to the . 9°N DNA polymerase, and that it can be developed into a continuous method for DNA sequencing with dNTP analogs carrying a 3'-ester with a fluorophore.

NLRP7 contributes to in vitro decidualization of endometrial stromal cells.

Background: Nucleotide-binding oligomerization domain (NACHT), leucine rich repeat (LRR) and pyrin domain (PYD) 7 containing protein, NLRP7, is a member of the NLR family which serves as innate immune sensors. Mutations and genetic variants of NLRP7 have been found in women with infertility associated conditions, such as recurrent hydatidiform mole, recurrent miscarriage, and preeclampsia. Decidualization of endometrial stromal cells is a hallmark of tissue remodeling to support embryo implantation and proper placental development.

Medroxyprogesterone acetate drives M2 macrophage differentiation toward a phenotype of decidual macrophage.

M1 macrophage differentiation plays a crucial role in enhanced inflammation during pregnancy, which may lead to pregnancy complications. Therefore, modulation of macrophage differentiation toward the M2 phenotype is desirable to ensure a successful pregnancy. Medroxyprogesterone acetate (MPA) is a potent progestin with an anti-inflammatory property, but its effect on macrophage differentiation is unknown.

Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth.

The development and differentiation of steroidogenic organs are controlled by Ad4BP/SF-1 (adrenal 4 binding protein/steroidogenic factor 1). Besides, lysosomal activity is required for steroidogenesis and also enables adrenocortical cell to survive during stress. However, the role of lysosomal activity on steroidogenic cell growth is as yet unknown.

MicroRNA miR-204 and miR-1236 inhibit hepatitis B virus replication via two different mechanisms.

Hepatitis B virus (HBV) is a major human pathogen. In this study, we found that miR-204 and miR-1236 were down-regulated in HBV-producing cells, and each could suppress HBV replication. Using a bioinformatic approach and a reporter assay, we identified miR-1236, which can reduce HBV replication and protein production by directly targeting at HBV specific mRNA.

Control and Eradication Strategies of Hepatitis B Virus.

Hepatitis B virus (HBV) is a major human pathogen, and chronic hepatitis can lead to cirrhosis and malignant hepatocellular carcinoma. While HBV vaccine and treatment are available, it has remained a challenge to completely eradicate the virus from patients. Current therapy using either interferon or polymerase inhibitors cannot cure HBV with a high efficacy.

A Common Variant of PROK1 (V67I) Acts as a Genetic Modifier in Early Human Pregnancy through Down-Regulation of Gene Expression.

PROK1-V67I has been shown to play a role as a modifier gene in the PROK1-PROKR system of human early pregnancy. To explore the related modifier mechanism of PROK1-V67I, we carried out a comparison study at the gene expression level and the cell function alternation of V67I, and its wild-type (WT), in transiently-transfected cells. We, respectively, performed quantitative RT-PCR and ELISA assays to evaluate the protein and/or transcript level of V67I and WT in HTR-8/SV neo, JAR, Ishikawa, and HEK293 cells.

MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ.

In hepatitis B virus (HBV)-replicating hepatocytes, miR-130a expression was significantly reduced. In a reciprocal manner, miR-130a reduced HBV replication by targeting at two major metabolic regulators PGC1α and PPARγ, both of which can potently stimulate HBV replication. We proposed a positive feed-forward loop between HBV, miR-130a, PPARγ, and PGC1α.

Prenatal diagnosis of Prader-Willi syndrome and Angelman syndrome for fetuses with suspicious deletion of chromosomal region 15q11-q13.

Objective: To identify Prader-Willi syndrome (PWS) and Angelman syndrome (AS) among fetuses with suspicious deletion of the chromosomal region 15q11-q13.

Methods: In a retrospective study, data were assessed from fetuses missing chromosomal band 15q12 that underwent molecular diagnosis at the National Chen-Kung University Hospital, Tainan, Taiwan, between January 2001 and December 2012. Amniocytes were subjected to molecular testing, including fluorescence in situ hybridization (FISH) analysis, methylation-specific PCR (M-PCR), and methylation-specific multiplex-ligation-dependent probe amplification (MS-MLPA).

A genetic association study of NLRP2 and NLRP7 genes in idiopathic recurrent miscarriage.

Study Question: Do gene polymorphisms of two members of the human innate immune sensor nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing proteins (NLRP) family, NLRP2 and NLRP7, confer susceptibility to idiopathic recurrent miscarriage (RM)?

Summary Answer: We found a significant association of a tag single-nucleotide polymorphism (SNP) of NLRP7 (rs26949) with idiopathic RM, while a tag SNP of NLRP2 (rs127868) showed a marginally significant association.

What Is Known Already: Human NLRP2 and NLRP7 have been suggested to be maternal effect genes, regulating early embryonic development and establishment of maternal imprints. Anecdotal evidence showed women who had experienced at least three consecutive miscarriages without hydatidiform mole carried non-synonymous NLRP7 variants.

Fas ligand enhances malignant behavior of tumor cells through interaction with Met, hepatocyte growth factor receptor, in lipid rafts.

Many late-stage cancer cells express Fas ligand (FasL) and show high malignancy with metastatic potential. We report here a novel signaling mechanism for FasL that hijacks the Met signal pathway to promote tumor metastasis. FasL-expressing human tumor cells express a significant amount of phosphorylated Met.

MicroRNA-22 can reduce parathymosin expression in transdifferentiated hepatocytes.

Pancreatic acinar cells AR42J-B13 can transdifferentiate into hepatocyte-like cells permissive for efficient hepatitis B virus (HBV) replication. Here, we profiled miRNAs differentially expressed in AR42J-B13 cells before and after transdifferentiation to hepatocytes, using chip-based microarray. Significant increase of miRNA expression, including miR-21, miR-22, and miR-122a, was confirmed by stem-loop real-time PCR and Northern blot analyses.

Extracellular matrix of glioblastoma inhibits polarization and transmigration of T cells: the role of tenascin-C in immune suppression.

Dense accumulations of T cells are often found in peritumoral areas, which reduce the efficiency of contact-dependent lysis of tumor cells. We demonstrate in this study that the extracellular matrix (ECM) produced by tumors can directly regulate T cell migration. The transmigration rate of several T cells including peripheral blood primary T cell, Jurkat, and Molt-4 measured for glioma cells or glioma ECM was consistently low.

Zap70 controls the interaction of talin with integrin to regulate the chemotactic directionality of T-cell migration.

Aberrant lymphocyte infiltration is crucial for many disorders such as tumor immune escape and autoimmunity. In this study, we have investigated T-cell migration in a three-dimensional collagen matrix containing tumor spheroids and by using micro-Slide chemotaxis and found that Zap70 regulates directionality during cell chemotaxis. Jurkat cells actively migrated toward SDF-1, nutrition, and spheroids of MCF-7 breast carcinoma cells embedded in collagen matrix.

Aberrant integrin activation induces p38 MAPK phosphorylation resulting in suppressed Fas-mediated apoptosis in T cells: implications for rheumatoid arthritis.

Delayed Fas-mediated apoptosis in T cells is associated with inflammatory diseases including rheumatoid arthritis (RA). CD3(+) T cells in RA synovia expressed high amounts of phospho-p38 MAPK. Exposure to RA synovial fluid or soluble collagen, a degradation product of extracellular matrix abundant in RA synovium, induced the phosphorylation of p38 MAPK in Jurkat T cells accompanied by resistance against Fas-mediated apoptosis.

Caspase-3 enhances lung metastasis and cell migration in a protease-independent mechanism through the ERK pathway.

Caspase-3 is known as a cysteine protease that primarily executes the cell death program. However, some tumors express higher levels of caspase-3 in positive correlation with malignancy. Here, we showed that caspase-3 can promote tumor metastasis in a protease-independent mechanism.

Phosphatidylinositol 3-kinase/Akt activation by integrin-tumor matrix interaction suppresses Fas-mediated apoptosis in T cells.

It has recently become apparent that the microenvironment made up of the extracellular matrix may affect cell signaling. In this study, we evaluated Fas-triggered apoptosis in T cells in contact with tumor cells, which resembles the cell-to-cell interactions found in tumor regions. Jurkat cells were less susceptible to the Fas-mediated apoptosis when cocultured with U118, HeLa, A549, and Huh-7 tumor cells.