OBJECTIVE: This study was to investigate the expression and significance of Integrins subunits in laryngeal squamous cell carcinoma (LSCC). METHOD: The expression of Integrins subunits was detected by cDNA microarray in 4 cases of primary LSCC tissues and corresponding adjacent normal tissues. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) were used to identify the different expression of Integrins subunits in 24 cases of primary LSCC tissues and corresponding adjacent normal tissues. RESULT: A cDNA microarray analysis revealed significant changes in the expression of Integrins subunits, with IntegrinalphaV, Integrinbeta8 being up-regulated and Integrinalpha8 being down-regulated. The result of RT-PCR was consistent with that of cDNA microarray. The mRNA levels of IntegrinalphaV and Integrinbeta8 were significantly higher in LSCC tissues than that in corresponding adjacent normal tissues (1.0131 +/- 0.4780 vs 0.7591 +/- 0.4678 for IntegrinalphaV, P<0.05, 1.7362 +/- 1.3849 vs 1.2267 +/- 0.9363 for Integrinbeta8, P<0.05). The mRNA levels of Integrinalpha8 were significantly lower in LSCC tissues than that in corresponding adjacent normal tissues (0.2646 +/- 0.2622 vs 0.5457 +/- 0.3827, P<0.05). CONCLUSION The expression of IntegrinalphaV, Integrinbeta8, Integrinalpha8 were significantly up-regulated or down-regulated in laryngeal squamous cell carcinoma, which may relate to tumorigenesis and development of laryngeal squamous cell carcinoma.
Aged ; Aged, 80 and over ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Humans ; Integrin alpha Chains ; genetics ; metabolism ; Integrin alphaV ; genetics ; metabolism ; Integrin beta Chains ; genetics ; metabolism ; Laryngeal Neoplasms ; metabolism ; pathology ; Male ; Middle Aged ; Neoplasm Proteins ; metabolism ; Neoplasm Staging

OBJECTIVETo investigate the effect of baicalein on proliferation and migration of multiple myeloma (MM) cell lines and its molecular mechanism.

METHODSThe MM cell line RPMI-8226 and U266 cells were used as the model, and treated with different concentration and time of baicalein the effect of baicalein on the MM cells proliferation was assessed by MTT assay. With or without baicalein or Interleukin-6 (IL-6) treatment, the β-catenin protein level was analyzed by immunofluorescence assay and western blot assay and mRNA levels of β-catenin, c-myc, cyclin D1 and integrin 7 gene by RT-PCR. Transwell chamber migration assay was used to detect the cells migration ability with different concentration of baicalein cultured.

RESULTSBaicalein inhibited the MM cell line RPMI 8226 and U266 cell proliferation in a dose- and time-dependent manner. It simultaneously inhibited β-catenin protein level to resist the effect of IL-6 on inducing MM cell proliferation, and resulted in decrease of β-catenin, c-myc, cyclinD1 and integrin β7 mRNA levels. Baicalein also decreased migration ability of MM cells in a dose-dependent manner by SDF-1.

CONCLUSIONBaicalein can inhibit MM cells proliferation and migration, and its molecular mechanisms are associated with inhibition of proliferation related genes β-catenin, c-myc, cyclin D1 and integrin β7 expression.

Antigens, CD ; metabolism ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Cyclin D1 ; metabolism ; Flavanones ; pharmacology ; Humans ; Integrin alpha Chains ; metabolism ; Interleukin-6 ; pharmacology ; Multiple Myeloma ; metabolism ; pathology ; Proto-Oncogene Proteins c-myc ; metabolism ; RNA, Messenger ; genetics ; beta Catenin ; metabolism

Antigens, CD ; metabolism ; CD3 Complex ; metabolism ; Celiac Disease ; complications ; Chromosome Aberrations ; Chromosomes, Human, Pair 9 ; Diagnosis, Differential ; Enteropathy-Associated T-Cell Lymphoma ; complications ; genetics ; metabolism ; pathology ; Humans ; Integrin alpha Chains ; metabolism ; Intestinal Mucosa ; pathology ; Ki-1 Antigen ; metabolism ; Lymphoma, Extranodal NK-T-Cell ; pathology ; Lymphoma, Large B-Cell, Diffuse ; pathology

Alcohol influences the neuroadaptation of brain cells where receptors and enzymes like protein kinase C (PKC) exist. Naltrexone acts on opioid receptors. However, other mechanisms of action remain unknown. We prepared SH-SY5Y neuroblastoma cells, and fed them with 150 mM ethanol for 72 h followed by treatment with naltrexone for 24 h. We performed microarray analysis and reverse transcriptase-polymerase chain reaction. Our results showed that PKC epsilon increased 1.90 times and showed an overall decreasing pattern as time increased. Phosphorylated ERK also increased 2.0 times according to the change of PKC epsilon. Integrin alpha7 increased 2.32 times and showed an increasing pattern as time increased. In conclusion, naltrexone influences PKC epsilon neuronal signaling system and endothelial adhesion molecule integrin alpha7 in addition to the well-known opioid system.
Antigens, CD/*metabolism ; Cell Line, Tumor ; Comparative Study ; DNA, Complementary/genetics ; Humans ; Integrin alpha Chains/*metabolism ; Naltrexone/*pharmacology ; *Neuroblastoma/enzymology/metabolism/pathology ; Oligonucleotide Array Sequence Analysis ; Protein Kinase C-epsilon/*metabolism ; Research Support, Non-U.S. Gov't ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors

To investigate the effect of the jianpi-jiedu formula (JPJD) on the expression of angiogenesis-relevant genes in colon cancer.
 Methods: Crude extract was obtained from JPJD by water extract method. The effect of JPJD crude extract on colon cancer cell proliferation capacity was determined by MTT assays. The IC50 value was calculated by GraphPad Prism5 software. Affymetrix gene expression profiling chip was used to detect significant differences in expressions of genes after JPJD intervention, and pathway enrichment analysis was performed to analyze the differentially expressed genes. Ingenuity Pathway Analysis software was applied to analyze differentially expressed genes relevant to tumor angiogenesis based on mammalian target of rapamycin (mTOR) signaling pathway and then the network diagram was built. Western blot was used to verify the protein levels of key genes related to tumor angiogenesis.
 Results: JPJD crud extract inhibited the proliferation capacity in colon cancer cells. The IC50 values in 24, 48, and 72 hours after treatment were 13.060, 9.646 and 8.448 mg/mL, respectively. The results of chip showed that 218 genes significantly upgraded, and 252 genes significantly downgraded after JPJD treatment. Most of the genes were related to the function of biosynthesis, metabolism, cell apoptosis, antigen extraction, angiogenesis and so on. There were 12 differentially expressed angiogenesis genes. IPA software analysis showed that the JPJD downregulated expression of sphingomyelin phosphodiesterase 3 (SMPD3), VEGF, vascular endothelial growth factor A (VEGFA), integrin subunit alpha 1 (ITGA1), cathepsin B (CTSB), and cathepsin S (CTSS) genes, while upregulated expressions of GAB2 and plasminogen activator, urokinase receptor (PLAUR) genes in the colorectal cancer cell. Western blot results demonstrated that JPJD obviously downregulated expressions of phospho-mTOR (P-mTOR), signal transducer and activator of transcription 3 (STAT3), hypoxia inducible factor-1α (HIF-1α), and VEGF proteins, while obviously upregulated the level of phospho-P53 (P-P53) protein.
 Conclusion: JPJD may inhibit colorectal tumor angiogenesis through regulation of the mTOR-HIF-1α-VEGF signal pathway.
Animals ; Blotting, Western ; Cathepsin B ; drug effects ; metabolism ; Cathepsins ; drug effects ; metabolism ; Cell Line, Tumor ; drug effects ; Colorectal Neoplasms ; blood supply ; genetics ; Down-Regulation ; Drugs, Chinese Herbal ; pharmacology ; Gene Expression Profiling ; methods ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; drug effects ; metabolism ; Integrin alpha Chains ; drug effects ; metabolism ; Neovascularization, Pathologic ; genetics ; Receptors, Urokinase Plasminogen Activator ; drug effects ; metabolism ; STAT3 Transcription Factor ; drug effects ; metabolism ; Signal Transduction ; Sphingomyelin Phosphodiesterase ; drug effects ; metabolism ; TOR Serine-Threonine Kinases ; drug effects ; metabolism ; Tumor Suppressor Protein p53 ; drug effects ; metabolism ; Up-Regulation ; Vascular Endothelial Growth Factor A ; drug effects ; metabolism