p60 is a subunit of katanin involved in microtubule-severing. Previous studies of p60 were primarily focused on microtubule regulation and cell cycle regulation. More recent research has demonstrated that katanin p60 possesses a function in prostate cancer bone metastasis; however, its role in breast cancer bone metastasis remains unclear. In the present study, immunohistochemistry was used to analyze the expression of katanin p60 in primary and bone metastatic breast cancer. The role of up- and downregulated katanin p60 was investigated using cell proliferation, and migration experiments. Overall, katanin p60 was highly expressed in breast cancer bone metastatic tissue compared with primary tumor tissue. In breast cancer cells, overexpression of katanin p60 inhibited cell proliferation, but promoted cell migration, whereas silencing katanin p60 expression promoted cell proliferation but inhibited cell migration. Overall, the present study indicated that katanin p60 serves a role in cell proliferation and migration, and thus may be a novel therapeutic target for prevention of breast cancer metastasis.

Survivin variants specific real time quantitative RT-PCR was developed to analyze their expression in 53 paired cancer and para-cancerous tissues, and the expression of the wild-type survivin protein was detected by immunohistochemistry. The results showed that survivin mRNA and protein were expressed in gastric cancer and para-cancerous tissues. The survivin-2B was dominantly expressed in para-cancerous tissues, whereas the survivin-DeltaEx3 was more frequently detected in cancer tissues. The positive rate of survivin-2a was 100% in both cancer and para-cancerous tissues, but its relative transcript expression level was not significantly increased in cancer tissues in comparison with para-cancerous tissues. The correlation analysis revealed that the expression of survivin-2a mRNA was significantly associated with that of total survivin (r (s)=0.4178, P=0.0018), whereas inversely to that of survivin-DeltaEX3 (r (s)=-0.4506, P=0.0007). It was suggested that survivin-2a may act as an antagonist of survivin-DeltaEX3. The balance between antiapoptotic survivin iso-forms and nonantiapoptotic ones may play an important role in tumorigenesis and tumor progression. Promising value is hinted to analyze survivin and its variants in tumor early diagnosis and distinguishing malignant tumors from benign ones.

Based on the potential therapeutic value in targeting metabolism for the treatment of cancer, an organic arsenical PDT-BIPA was fabricated, which exerted selective anti-cancer activity in vitro and in vivo via targeting lactate dehydrogenase A (LDHA) to remodel the metabolic pathway. In details, the precursor PDT-BIPA directly inhibited the function of LDHA and converted the glycolysis to oxidative phosphorylation causing ROS burst and mitochondrial dysfunction. PDT-BIPA also altered several gene expression, such as HIF-1α and C-myc, to support the metabolic remodeling. All these changes lead to caspase family-dependent cell apoptosis in vivo and in vitro without obvious side effect. Our results provided this organic arsenical precursor as a promising anticancer candidate and suggested metabolism as a target for cancer therapies.decisions through the regulation of metabolic enzymes [3]. Researchers showed immense interest of getting agents which could selectively eradicate cancer cells by altering metabolism [4]. However, few specific LDHA inhibitors complied with the envisaging results in vivo. Oxamate, a pyruvate analog that inhibits LDH activity by blocking the pyruvate binding site, is a weak inhibitor (IC 50~8 00 µM) and lacks selectivity. GNE-140 is a selective LDHA inhibitor of nano-molar potency but if it is removed from the medium, cells can proliferate even after 2 d of continuous inhibition which implies that sustained inhibition is needed for long-term cancer cell control [5]. Despite multiple efforts from researchers all around the world to discover potent inhibitors of LDHA, few viable inhibitors [1,[6][7][8][9][10] emerged except pioneering work of GSK and Genentech. Their cellular effects or in vivo activity did not meet the clinical demands in spite of the potent biochemical activity [7].Here, we report that reduction of LDHA by a synthesized organic arsenical causes bioenergetic and oxidative stress leading to cell apoptosis. The synthesized organic arsenical (PDT-BIPA) carrying the S-As-S displayed the best inhibition rates (IC 50/24 h = 0.55 ± 0.01 µM) for HL-60 cells among six cancer cell lines. PDT-BIPA can inhibit LDHA in HL-60 cells in a concentration-and time-dependent way leading to the burst of ROS and metabolic changes to suppress cancer cells and tumor in vitro and in vivo, respectively. Moreover, this compound manifested different inhibitory mechanism toward leukemia with our previous work [11,12].

The purpose of this study was to quantify hepatitis B virus DNA by direct real-time PCR from serum without the need for DNA extraction. Crossing point (Cp) values were determined automatically using the second derivative maximum mode. Since serum samples from patients are inevitably haemolysed, lipaemic or icteric, the interference of endogenous substances from the serum in real-time PCR was evaluated. The result showed that, although serum protein quenched the intensity of fluorescence, the Cp value adopted to calculate the quantity of DNA copies remained unchanged. Importantly, real-time PCR from serum with or without DNA extraction reached a high level of concordance. This direct serum PCR method without the DNA extraction and gel electrophoresis allows for substantial labour and cost savings. In addition, it is also suitable for rapid DNA quantification during clinical diagnosis.