TRPM7 regulates the migration of human nasopharyngeal carcinoma cell by mediating Ca(2+) influx.
نویسندگان
چکیده
Ion channels are involved in various physiologic and pathologic processes, including the migration of tumor cells that is required for metastasis. To determine whether transient receptor potential melastatin 7 (TRPM7) Ca(2+) channels play an important role in the migration of tumor cells, we examined the potential function of TRPM7 channels in the migration of 5-8F and 6-10B human nasopharyngeal carcinoma cells. The migratory potential of 5-8F cells was significantly decreased by extracellular Ca(2+) chelator (EGTA), TRPM7 inhibitors (La(3+), 2-APB), or TRPM7 knockdown. Conversely, the addition of TRPM7 activator Bradykinin and overexpression of TRPM7 promoted the migration of 5-8F and 6-10B cells. Furthermore, the sustained Ca(2+) influx regulated by TRPM7 activated release of Ca(2+) stores via ryanodine receptors by a calcium-induced calcium release (CICR) mechanism. This study suggests, first, that Ca(2+) influx is required for the migration of human nasopharyngeal carcinoma 5-8F cells. Second, and more importantly, it identifies TRPM7 as a novel potential-regulator of the Ca(2+) influx that allows migration of 5-8F cells. TRPM7, therefore, might have potential as a prognostic indicator and as a therapeutic target in nasopharyngeal carcinoma.
منابع مشابه
microRNA-29a functions as a tumor suppressor in nasopharyngeal carcinoma 5-8F cells through targeting VEGF
Objective(s): microRNA-29 (miR-29) family miRNAs have been mentioned as tumor suppressive genes in several human cancers. The purpose of this study was to investigate the function of miR-29a in nasopharyngeal carcinoma (NPC) cells. Materials and Methods: Human NPC cell line 5-8F was transfected with mimic, inhibitor or scrambled controls...
متن کاملTRPM7-mediated Ca2+ signals confer fibrogenesis in human atrial fibrillation.
RATIONALE Cardiac fibrosis contributes to pathogenesis of atrial fibrillation (AF), which is the most commonly sustained arrhythmia and a major cause of morbidity and mortality. Although it has been suggested that Ca(2+) signals are involved in fibrosis promotion, the molecular basis of Ca(2+) signaling mechanisms and how Ca(2+) signals contribute to fibrogenesis remain unknown. OBJECTIVE To ...
متن کاملTRPC1 functions as a store-operated Ca2+ channel in intestinal epithelial cells and regulates early mucosal restitution after wounding.
An increase in cytosolic free Ca(2+) concentration ([Ca(2+)](cyt)) results from Ca(2+) release from intracellular stores and extracellular Ca(2+) influx through Ca(2+)-permeable ion channels and is crucial for initiating intestinal epithelial restitution to reseal superficial wounds after mucosal injury. Capacitative Ca(2+) entry (CCE) induced by Ca(2+) store depletion represents a major Ca(2+)...
متن کاملCircRNA_0109291 regulates cell growth and migration in oral squamous cell carcinoma and its clinical significance
Objective(s): Circular RNAs (circRNAs), a new class of non-coding RNAs, have emerged as important regulators during tumorigenesis. However, the functions of circRNAs have not been completely clarified in the progression of cancers. In our study, a novel circRNA hsa_circ_0109291 was investigated in oral squamous cell carcinoma (OSCC) tissues and cell lines. Materials and Methods: The expression ...
متن کاملImportance of melastatin-like transient receptor potential 7 and magnesium in the stimulation of osteoblast proliferation and migration by platelet-derived growth factor.
Bone is a dynamic tissue that is continuously being remodeled throughout life. Specialized cells called osteoclasts transiently break down old bone (resorption process) at multiple sites as other cells known as osteoblasts are replacing it with new tissue (bone formation). Usually, both resorption and formation processes are in balance and thereby maintain skeletal strength and integrity. This ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Cell calcium
دوره 47 5 شماره
صفحات -
تاریخ انتشار 2010