Purpose: To observe the apoptotic effects of NSMF on human hepatoma cells and to investigate the mechanisms. Materials and methods: Human hepatoma cell line Bel-7402 and Hep G-2 were treated by 0.2 T rotary NSMF (30 min/d) with 250 Hz, 400 Hz and 500 Hz for 3 d and 6 d, respectively. Apoptosis was analyzed with flow cytometry. Cell proliferation was measured with XTT assay. Expression of Bcl-2, caspase3/8/9 was analyzed with ELISA. Results: After 6 d treatment, significant apoptosis was induced by 400 Hz in Bel-7402 cells. Slight cell apoptosis was observed at 250 Hz, while Hep G-2 cells exhibited slight apoptosis at 250 Hz and 400 Hz. After 3 d treatment, no apoptosis exhibited in both cell types. Compared with control group, expression of Bcl-2 and Caspase 8 in treated Bel-7402 cells were significantly reduced (p < 0.01), while Caspase 3 and Caspase 9 were significantly upregulated (p < 0.01). Conclusions: NSMF upregulates caspase 9 and downregulates Bel-2 expression, which results in higher level of active caspase 3 to trigger apoptosis in cells. Different cell types require different NSMF factors like rotary frequency and treatment time to induce apoptosis.

Pancreatic ductal adenocarcinoma (PDAC) remains a clinical challenge due to its poor prognosis. Therefore, the early diagnosis of PDAC is extremely important for achieving a cure. MicroRNAs (miRNAs)...

ATP binding cassette (ABC) transporters can transfer a variety of antiviral agents from the cytoplasm to body fluid, which results in a reduced intracellular concentration of the drugs. Proteins of HIV-1, e.g., Tat and gp120, altered some types of ABC transporter expression in brain microvascular endothelial cells and astrocytes. However, the effect of Tat on ABC transporters in T lymphocytes is unclear. In this study the status of breast cancer resistance protein (BCRP) in Tat expressing cell lines was examined with real-time PCR and flow cytometry. It was found that HIV-1 Tat protein upregulated BCRP expression and enhanced efflux mediated by BCRP significantly, which could inhibit antiviral drugs from entering infected cells and interfere with the therapeutic effect of HAART.

The bovine immunodeficiency virus (BIV) transactivator (BTat) recruits the bovine cyclin T1 (B-cyclin T1) to the LTR to facilitate the transcription of BIV. Here, we demonstrate that bovine hexamethylene bisacetamide (HMBA)-induced protein 1 (BHEXIM1) inhibits BTat-mediated BIV LTR transcription. The results of in vivo and in vitro assays show direct binding of BHEXIM1 to the B-cyclin T1. These results suggest that the repression arises from BHEXIM1-BTat competition for B-cyclin T1, which allows BHEXIM1 to displace BTat from B-cyclin T1. Furthermore, we found that the C-terminal region and the centrally located region of BHEXIM1 are required for BHEXIM1 to associate with B-cyclin T1. Knockdown of BHEXIM1 enhances BIV replication. Taken together, our study provides the first clear evidence that BHEXIM1 is involved in BIV replication through regulating BTat-mediated transactivation.

Pancreatic Ductal Adenocarcinoma (PDAC) is a disease with high mortality rates due to metastasis. Epithelial-Mesenchymal Transition (EMT) is correlated with metastasis and drug resistance in PDAC. Therefore, elucidating the changes in cellular characteristics in PDAC before and after EMT is essential to understand EMT in PDAC cells and to develop novel therapeutic methods for PDAC. The human PDAC cell line Panc-1 was used to measure cell stiffness before and after EMT induction by TGF-β. EMT biomarker expression levels were measured to identify cell status using real-time PCR, immune cytochemistry. Changes in cell stiffness before and after EMT were investigated by Atomic Force Microscope with Young’s modulus. Cell size was determined by image analysis. Cellular lipids were examined. Expression levels of lamin A, the gene associated with cell stiffness, were quantified by real-time PCR. After induced EMT, PDAC cells were stiffer with larger cell sizes than before EMT. The expression levels of cytoskeletal proteins did not change significantly, but lamin A expression was significantly reduced after EMT. The amount of polyunsaturated fatty acids in the cell membrane increased, while monounsaturated fatty acids decreased. We reported the changes of cell stiffness and other biological characteristics in PDAC cells after EMT. Cell stiffness was determined by multiple factors before and after EMT. These results provide new directions for understanding EMT in PDAC, which is critical for developing new therapies for PDAC.