No abstract

No abstract

No abstract

No abstract

This study reports possible interferences for the detection of NO2− on a Au–G–PANI/GCE.

B-lymphocyte stimulator (BAFF) is a recently recognized member of the tumor necrosis factor ligand family (TNF) and a potent cell-survival factor expressed in many hematopoietic cells. BAFF regulates B-cell survival, differentiation, and proliferation by binding to three TNF receptors: TACI, BCMA, and BAFF-R. The mechanism involved in BAFF-R gene expression and regulation remains elusive. In this study, we examined BAFF-R gene expression, function, and regulation in multiple myeloma (KM3) cells. It was found that BAFF-BAFF-R induced cell survival by activating NF-κB1 pathway and NF-κB2 pathway. It was also found that NF-κB was an important transcription factor involved in regulating BAFF-R expression through one NF-κB binding site in the BAFF-R promoter, suggesting that inhibiting NF-κB could decrease the expression of BAFF-R mRNA and protein, and promote activity of BAFF-R gene. Our findings indicate that both NF-κB pathways are involved in the regulation of BAFF-R gene and the NF-κB-binding site of BAFF-R may be a new therapeutic target in this disease.

Cancerous inhibitor of protein phosphatase 2A (CIP2A) has been identified as an oncoprotein that is able to promote the proliferation of cancer cells. The role of CIP2A in the anticancer activity of bortezomib in colon cancer remains to be elucidated. In the present study, the antitumor effect of bortezomib was investigated and the role of CIP2A in determining the effect on colon cancer cells was identified. In the present study, bortezomib demonstrated an antitumor effect, as observed by WST‑1 assay and flow cytometry. In addition, the mRNA and protein level of CIP2A was inhibited in a dose‑dependent manner by bortezomib with quantitative PCR (qPCR) and western blotting. Furthermore, the inhibition of CIP2A with small interfering RNA by treatment with bortezomib inhibited proliferation, increased apoptosis and attenuated the invasion of the cells. Finally, the in vivo data demonstrated that bortezomib was able to decrease the growth of tumors, and that CIP2A was downregulated in the LoVo tumors treated with bortezomib. Therefore, CIP2A was shown to be important in the bortezomib‑induced inhibitory effect on colon cancer.

Ordered mesoporous g-C3N4, synthesized via a green cosolvent-free nanocasting route, exhibited remarkable photodegradation performance towards methyl orange with a degradation rate constant 30 times higher than that of bulk g-C3N4.