Abstract.It is well known that local anesthetics have a broad spectrum of pharmacological actions, acting as nerve blocks, and treating pain and cardiac arrhythmias via blocking of the sodium channel. The use of local anesthetics could reduce the possibility of cancer metastasis and recurrence following surgical tumor excision. The purpose of the present study was to investigate the inhibitory effect of lidocaine upon the invasion and migration of transient receptor potential cation channel subfamily V member 6 (TRPV6)-expressing cancer cells. Human breast cancer MDA-MB-231 cells, prostatic cancer PC-3 cells and ovarian cancer ES-2 cells were treated with lidocaine. Cell viability was quantitatively determined by MTT assay. The migration of the cells was evaluated using the wound healing assay, and the invasion of the cells was assessed using a Transwell assay. Calcium (Ca 2+ ) measurements were performed using a Fluo-3 AM fluorescence kit. The expression of TRPV6 mRNA and protein in the cells was determined by quantitative-polymerase chain reaction and western blot analysis, respectively. The results suggested that lidocaine inhibits the cell invasion and migration of MDA-MB-231, PC-3 and ES-2 cells at lower than clinical concentrations. The inhibitory effect of lidocaine on TRPV6-expressing cancer cells was associated with a reduced rate of calcium influx, and could occur partly as a result of the downregulation of TRPV6 expression. The use of appropriate local anesthetics may confer potential benefits in clinical practice for the treatment of patients with TRPV6-expressing cancer.

This paper presents a passive wireless humidity sensor for concrete monitoring. After discussing the transmission of electromagnetic wave in concrete, a novel architecture of wireless humidity sensor, based on Ultra-High Frequency (UHF) Radio Frequency Identification (RFID) technology, is proposed for low-power application. The humidity sensor utilizes the top metal layer to form the interdigitated electrodes, which were then filled with polyimide as the humidity sensing layer. The sensor interface converts the humidity capacitance into a digital signal in the frequency domain. A two-stage rectifier adopts a dynamic bias-voltage generator to boost the effective gate-source voltage of the switches in differential-drive architecture. The clock generator employs a novel structure to reduce the internal voltage swing. The measurement results show that our proposed wireless humidity can achieve a high linearity with a normalized sensitivity of 0.55% %RH at 20 °C. Despite the high losses of concrete, the proposed wireless humidity sensor achieves reliable communication performances in passive mode. The maximum operating distance is 0.52 m when the proposed wireless sensor is embedded into the concrete at the depth of 8 cm. The measured results are highly consistent with the results measured by traditional methods.

Autophagy and ER stress participated in the inhibition of MPPa‐PDT on tumor growth, but the molecular links between them remain undefined. We just explore the molecular mechanism between them in vitro and vivo. CCK‐8 assay and flow cytometer were used to detect the cytotoxicity and mode of cell death after MPPa‐PDT. Furthermore, the role of autophagy was verified in MPPa‐PDT. Confocal microscopy was used to show the intracellular distribution of MPPa. ER stress markers and PERK signaling pathway were detected by western blot. While in vivo, tumor histology and immunohistochemistry were performed to show the effect of MPPa‐PDT in mice. After MPPa‐PDT, cells viability decreased in dose‐dependent manner. Besides, the cell apoptosis increased along with the increasing of Beclin‐1and LC3B II but declining of P62. When pretreated with 3‐MA, LC3B II formation and the cytotoxicity declined. MPPa‐PDT caused increasing of ER stress markers (GRP78, CHOP) as MPPa accumulated in ER. However, pretreatment with ER stress inhibitor 4PBA, the expression of GRP78 and LC3B II was blocked but the PERK signaling pathway activated and the expression of P62 increased. In vivo, the tumor growth was significantly inhibited by MPPa‐PDT. Besides, the appearance of ER stress and autophagy was further demonstrated by immunohistochemistry. Our findings demonstrate that autophagy mediated by MPPa‐PDT was regulated by ER stress, via PERK signaling pathway, to kill MDA‐MB‐231 cells in vitro and vivo.

BackgroundBreast cancer is one of the most commonly diagnosed cancers in women, with high morbidity and mortality. Tumor metastasis is implicated in most breast cancer deaths; thus, inhibiting metastasis may provide a therapeutic direction for breast cancer. In the present study, pyropheophorbide-α methyl ester-mediated photodynamic therapy (MPPa-PDT) was used to inhibit metastasis in MCF-7 breast cancer cells.MethodsUptake of MPPa was detected by fluorescence microscopy. Cell viability was evaluated by the Cell Counting Kit-8 (CCK-8). ROS generation was detected by 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA). The migration of cells was assessed by wound healing assay, and invasion ability was assessed by Matrigel invasion assay. Levels of MMP2 and MMP9 were measured by PCR. Akt, phospho-Akt (Ser473), phospho-NF-κB p65 (Ser536) and NF-κB p65 were measured by western blotting. The F-actin cytoskeleton was observed by immunofluorescence. Lung tissue was visualized by hematoxylin and eosin staining.ResultsFollowing MPPa-PDT, migration and invasion were decreased in the MCF-7 cells. MPPa-PDT downregulated the expression of MMP2 and MMP9, which are responsible for the initiation of metastasis. MPPa-PDT reduced the phosphorylation of Akt and NF-κB. MPPa-PDT also reduced the expression of F-actin in cytoskeleton in MCF-7 cells. These effects were blocked by the reactive oxygen species scavenger NAC or the Akt activator SC79, while the PI3K inhibitor LY294002 or the Akt inhibitor triciribine enhanced these effects. Moreover, MPPa-PDT inhibited tumor metastasis and destroyed F-actin in vivo.ConclusionTaken together, these results demonstrate that MPPa-PDT inhibits the metastasis of MCF-7 cells both in vitro and in vivo and may be involved in the Akt/NF-κB-dependent MMP-9 signaling pathway. Thus, MPPa-PDT may be a promising treatment to inhibit metastasis.

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