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This corrects the article DOI: 10.1038/onc.2014.43.
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B-cell lymphoma/leukemia 10 (BCL10) is an apoptotic regulatory protein related to advanced TNM stage and disease recurrence in oral squamous cell carcinoma (OSCC). However, the regulatory mechanism of BCL10 in OSCC progression is still unknown. Here, we showed that knockdown of endogenous BCL10 could significantly reduce cell migration and invasion abilities, retard cell proliferation by G0/G1 phase accumulation and inhibit tumorigenicity in vivo. In molecular level, we identified S100P as a crucial downstream effector of BCL10-inhibited OSCC progression by high-throughput microarray analysis. S100P messenger RNA and protein expression levels were significantly diminished in silenced-BCL10 clones, and transfected S100P expression plasmids restored migration, invasion, proliferation abilities and tumorigenicity in shBCL10 transfectants. Furthermore, we provided evidence that BCL10 regulated S100P expression through signal transducers and activators of transcription 1 (STAT1) and activating transcription factor 4 (ATF4). Knockdown of BCL10 decreased S100P promoter activity, but showed no effect in truncated STAT1/ATF4 S100P promoter. In addition, we also found that the P50/P65 signaling pathway was involved in BCL10-enhanced OSCC progression. Restored S100P in silenced-BCL10 clones could markedly reverse P65 activation via outside-in signaling. Taken together, we discovered a novel axis of BCL10-regulated OSCC progression via STAT1/ATF4/S100P/P65 signaling, which could predict the prognosis of OSCC and will be beneficial for developing therapeutic strategy against advanced OSCC.
Asunto(s)
Factor de Transcripción Activador 4/metabolismo , Proteínas Adaptadoras Transductoras de Señales/metabolismo , Proteínas de Unión al Calcio/metabolismo , Neoplasias de la Boca/metabolismo , Proteínas de Neoplasias/metabolismo , Factor de Transcripción STAT1/metabolismo , Transducción de Señal , Factor de Transcripción Activador 4/genética , Proteínas Adaptadoras Transductoras de Señales/genética , Animales , Proteína 10 de la LLC-Linfoma de Células B , Sitios de Unión , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular , Transformación Celular Neoplásica/genética , Transformación Celular Neoplásica/metabolismo , Modelos Animales de Enfermedad , Progresión de la Enfermedad , Técnicas de Silenciamiento del Gen , Xenoinjertos , Humanos , Ratones , Neoplasias de la Boca/genética , Neoplasias de la Boca/mortalidad , Neoplasias de la Boca/patología , Pronóstico , Unión Proteica , Activación TranscripcionalRESUMEN
A portable multichannel system is described for the recording of biomedical signals wirelessly. Instead of using the conversional time-division analog-modulation method, the technique of digital multiplexing was applied to increase the number of signal channels to 4. Detailed design considerations and functional allocation of the system is discussed. The frontend unit was modularly designed to condition the input signal in an optimal manner. Then, the microcontroller handled the tasks of data conversion, wireless transmission, as well as providing the ability of simple preprocessing such as waveform averaging or rectification. The low-power nature of this microcontroller affords the benefit of battery operation and hence, patient isolation of the system. Finally, a single-chip receiver, which compatible with the RF transmitter of the microcontroller, was used to implement a compact interface with the host computer. An application of this portable recorder for low-back pain studies is shown. This device can simultaneously record one ECG and two surface EMG wirelessly, thus, is helpful in relieving patients' anxiety devising clinical measurement. Such an approach, microcontroller-based wireless measurement, could be an important trend for biomedical instrumentation and we help that this paper could be useful for other colleagues.
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The validity of the fibromyalgia syndrome (FMS) as a distinct clinical entity has been challenged for several reasons. Many skeptics express concern about the subjective nature of chronic pain, the subjectivity of the tender point (TeP) examination, the lack of a gold standard laboratory test, and the absence of a clear pathogenic mechanism by which to define FMS. Another expressed concern has been the relative nature of the pain-distress relationship in the rheumatology clinic. The apparently continuous relationship between TePs and somatic distress across a variety of clinical disorders is said to argue against FMS as a separate clinical disorder. The most aggressive challenges of the FMS concept have been from legal defenses of insurance carriers motivated by economic concerns. Other forms of critique have presented as psychiatric dogma, uninformed posturing, suspicion of malingering, ignorance of nociceptive physiology, and occasionally have resulted from honest misunderstanding. It is not likely that a few paragraphs of data and logic will cause an unbeliever to change an ingrained opinion. Therefore, this review describes the clinical manifestations of FMS, responds to some of the theoretic arguments against it, and discusses some possible pathophysiologic mechanisms by which FMS may develop and persist as a unique syndrome.