Suppression of 14-3-3γ-mediated surface expression of ANO1 inhibits cancer progression of glioblastoma cells

Lee, Jae Kwang; Bae, Yeonju; Lee, Bok Soon; Kim, Eunju; Cho, Chang Hoon; Ryoo, Kanghyun; Yoo, Ji Myong; Kim, Chul Ho; Yi, Gwan Su; Lee, Seok-Geun; Lee, C. Justin; Kang, Sang Soo; Hwang, Eun Mi; Park, Jae Yong

doi:10.1038/srep26413

Cited by 45 publications

(43 citation statements)

References 53 publications

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“…Therefore, we suggest that the mHb-IPN-DRN pathway may be directly involved in social behaviors, a notion that should be further investigated. Since the activities of TMEM16A can be regulated via protein-protein interactions [63,64], it will be worth examining whether and how TMEM16A-interacting proteins may regulate the neuronal excitability of the mHb. Therefore, we propose that TMEM16A could be a novel target for therapeutics against anxiety-related disorders.…”

Section: Chemogenetic Inhibition Of the Cholinergic Neurons In The Mhmentioning

confidence: 99%

TMEM16A expression in cholinergic neurons of the medial habenula mediates anxiety‐related behaviors

et al. 2019

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TMEM16A, a Ca 2+ -activated Cl À channel, is known to modulate the excitability of various types of cells; however, its function in central neurons is largely unknown. Here, we show the specific expression of TMEM16A in the medial habenula (mHb) via RNAscope in situ hybridization, immunohistochemistry, and electrophysiology. When TMEM16A is ablated in the mHb cholinergic neurons (TMEM16A cKO mice), the slope of after-hyperpolarization of spontaneous action potentials decreases and the firing frequency is reduced. Reduced mHb activity also decreases the activity of the interpeduncular nucleus (IPN). Moreover, TMEM16A cKO mice display anxiogenic behaviors and deficits in social interaction without despair-like phenotypes or cognitive dysfunctions. Finally, chemogenetic inhibition of mHb cholinergic neurons using the DREADD (Designer Receptors Exclusively Activated by Designer Drugs) approach reveals similar behavioral phenotypes to those of TMEM16A cKO mice. We conclude that TMEM16A plays a key role in anxiety-related behaviors regulated by mHb cholinergic neurons and could be a potential therapeutic target against anxiety-related disorders.Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala. Nature 537: 97 -101 ª 2019 The Authors EMBO reports 21: e48097 | 2020

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Section: Chemogenetic Inhibition Of the Cholinergic Neurons In The Mhmentioning

confidence: 99%

TMEM16A expression in cholinergic neurons of the medial habenula mediates anxiety‐related behaviors

et al. 2019

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“…Although TMEM16A overexpression does not affect cell migration in HEK293 cells [ 94 ], TMEM16A promotes cell migration and invasion in various tumors such as HNSCC, hepatocellular carcinoma, lung cancer, glioblastoma, gastric cancer, pancreatic ductal adenocarcinoma, glioma, oral squamous cell carcinoma, and CRC [ 45 , 46 , 48 , 51 , 52 , 54 , 56 , 92 , 96 , 97 ] (Table 1 ), as well as in non-tumor cells such as bronchial epithelial cells [ 98 ] and Ehrlich Lettre ascites (ELA) cells [ 99 ]. Interestingly, Jacobsen et al found that TMEM16A knockdown resulted in a change in the migrating direction in ELA cells, whereas TMEM16F knockdown reduced the speed of migration [ 99 ].…”

Section: Introductionmentioning

confidence: 99%

Cell-specific mechanisms of TMEM16A Ca2+-activated chloride channel in cancer

et al. 2017

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TMEM16A (known as anoctamin 1) Ca2+-activated chloride channel is overexpressed in many tumors. TMEM16A overexpression can be caused by gene amplification in many tumors harboring 11q13 amplification. TMEM16A expression is also controlled in many cancer cells via transcriptional regulation, epigenetic regulation and microRNAs. In addition, TMEM16A activates different signaling pathways in different cancers, e.g. the EGFR and CAMKII signaling in breast cancer, the p38 and ERK1/2 signaling in hepatoma, the Ras-Raf-MEK-ERK1/2 signaling in head and neck squamous cell carcinoma and bladder cancer, and the NFκB signaling in glioma. Furthermore, TMEM16A overexpression has been reported to promote, inhibit, or produce no effects on cell proliferation and migration in different cancer cells. Since TMEM16A exerts different roles in different cancer cells via activation of distinct signaling pathways, we try to develop the idea that TMEM16A regulates cancer cell proliferation and migration in a cell-dependent mechanism. The cell-specific role of TMEM16A may depend on the cellular environment that is predetermined by TMEM16A overexpression mechanisms specific for a particular cancer type. TMEM16A may exert its cell-specific role via its associated protein networks, phosphorylation by different kinases, and involvement of different signaling pathways. In addition, we discuss the role of TMEM16A channel activity in cancer, and its clinical use as a prognostic and predictive marker in different cancers. This review highlights the cell-type specific mechanisms of TMEM16A in cancer, and envisions the promising use of TMEM16A inhibitors as a potential treatment for TMEM16A-overexpressing cancers.

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“…Baine MJ et al reported that the level of coagulation factor V was found to be significantly different in an analysis of peripheral monocytes from pancreatic cancer patients and might be related to tumor stage [22]. YWHAG is a member of a highly conserved family of proteins that participates in many intracellular signal transduction processes and plays an important role in cell survival and proliferation [23][24][25][26]. However, the role of YWHAG in pancreatic Fig.…”

Section: Discussionmentioning

confidence: 99%

Identification of dissociation factors in pancreatic Cancer using a mass spectrometry-based proteomic approach

et al. 2020

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Backgroud: Pancreatic cancer is a highly malignant tumor of the digestive system. This secretome of pancreatic cancer is key to its progression and metastasis. But different methods of protein extraction affect the final results. In other words, the real secretion of proteins in cancer cells has been changed. Based on mass spectrometry, we analyze the secretome from the serum-containing and serum-free medium, using different protein pretreatment methods. This study aims to identify dissociation factors in pancreatic cancer. Methods: In this study, pancreatic cancer cells were cultured in serum-containing or serum-free medium, and the corresponding supernatants were extracted as samples. Subsequently, the above samples were separated by size exclusion chromatography (SEC), and peptide segments were identified by LC-MS/MS. The final results were identified via the hamster secreted protein database and a public database. Results: Although the number of identified proteins in the serum-free medium group was high, the real secretion of proteins in pancreatic cancer cells was changed. There were six significant secreted proteins in the serumcontaining medium group. Survival analysis via the TCGA database suggested that patients with higher expression levels of YWHAG showed a worse overall survival rate than those with lower YWHAG expression. Conclusions: Our study demonstrated the results in the serum-containing medium group were more similar to the real secretome of pancreatic cancer cells. YWHAG could be used as a prognostic indicator for pancreatic cancer.

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Suppression of 14-3-3γ-mediated surface expression of ANO1 inhibits cancer progression of glioblastoma cells

Cited by 45 publications

References 53 publications

TMEM16A expression in cholinergic neurons of the medial habenula mediates anxiety‐related behaviors

TMEM16A expression in cholinergic neurons of the medial habenula mediates anxiety‐related behaviors

Cell-specific mechanisms of TMEM16A Ca2+-activated chloride channel in cancer

Identification of dissociation factors in pancreatic Cancer using a mass spectrometry-based proteomic approach

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