scholarly journals Rab11 is essential for lgl mediated JNK–Dpp signaling in dorsal closure and epithelial morphogenesis in Drosophila

2019 ◽  
Author(s):  
Nabarun Nandy ◽  
Jagat Kumar Roy
Keyword(s):  
Signaling Pathway ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Epithelial Morphogenesis ◽  
Dorsal Closure ◽  
Cellular Mechanisms ◽  
Epithelial Wound Healing ◽  
Spatio Temporal ◽  
Targeted Gene Expression ◽  
Shape Changes

AbstractDorsal closure in Drosophila provides a robust genetic platform providing deep insights into the basic cellular mechanisms that govern epithelial wound healing and morphogenesis. As dorsal closure proceeds, the adjacent epithelia advance contra-laterally involving coordinated cell shape changes in order to successfully accomplish the process. The JNK-Dpp signaling in these cells plays an instrumental role in guiding their fate as gastrulation completes. A huge number of genes have been reported to be involved in the regulation of this core signaling pathway, yet the mechanisms by which they do so is hitherto unclear, which forms the objective of our present study. Here we show that lgl, which is a potent tumour suppressor gene, conserved across the phyla till humans, regulates the JNK–Dpp pathway in the dorsal closure and epithelial morphogenesis process where in ectopic knockdown of this gene results in the failure of dorsal closure. Interestingly, we also find Rab11 to be interacting with lgl as they together regulate the core JNK-Dpp signaling pathway during dorsal closure and also during pupal thorax closure process. Using the robust Gal4-UAS system of targeted gene expression, we show here that Rab11 and lgl synergize to successfully execute the dorsal closure and the similar thorax closure process, ensuring proper spatio-temporal JNK-Dpp signaling.

scholarly journals Mir-20a-5p induced WTX deficiency promotes gastric cancer progressions through regulating PI3K/AKT signaling pathway

2020 ◽  
Author(s):  
Jian Li ◽  
Danli Ye ◽  
Peng Shen ◽  
Xiaorong Liu ◽  
Peirong Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Mtor Signaling ◽  
Tumour Suppressor ◽  
Mtor Signaling Pathway

Abstract Background: The X-linked gene WTX (also called AMER1) has been reported to function as a tumour suppressor gene in Wilms’ tumour. In our previous study, WTX expression was shown to be significantly reduced in gastric cancer (GC), but the function and mechanism associated with WTX loss had yet to be fully elucidated. Methods: WTX expression and clinical significance were father analyzed in GC and control normal gastric tissues, and validated in public databases. The candidate pathway which was regulated by WTX during GC progression was searched by KEGG pathway analysis. The miRNA which monitored WTX expression was screened by miRNA microarray. After verified the pathway and miRNA both in vitro and in vivo, the relationship of miRNA, WTX and the downstream pathway were analyzed by Western blot, immunohistochemistry, RT-PCR, Co-immunoprecipitation (Co-IP), and luciferase analyses.Results: The results showed that WTX serves as a tumour suppressor gene in GC. The loss of WTX which is associated with the aggressiveness of GC by promoting GC cell proliferation in vitro and high metastasis in vivo. Furthermore, WTX expression was positively correlated with the overall survival of GC patients. Microarray assays, bioinformatics analysis, and verification experiments showed that WTX loss activates the PI3K/AKT/mTOR pathway and promotes GC cell proliferation and invasion. And the aberrant miR-20a-5p upregulation contributes to WTX loss in GC, which stimulates PI3K phosphorylation to activate PI3K/AKT/mTOR signaling pathway and promoted GC progression.Conclusions: The results of the present study elucidated the mechanism of GC progression, which is at least partially caused by aberrant miR-20a-5p upregulation leading to the inhibition of WTX expression and PI3K/AKT/mTOR signaling pathway activation. These findings provide a comprehensive understanding of the action of the miR-20a-5p/WTX/PI3K/AKT/mTOR signaling pathway in the progression and metastasis of GC.

scholarly journals Mir-20a-5p induced WTX deficiency promotes gastric cancer progressions through regulating PI3K/AKT signaling pathway

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Jian Li ◽  
Danli Ye ◽  
Peng Shen ◽  
Xiaorong Liu ◽  
Peirong Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Mtor Signaling ◽  
Tumour Suppressor ◽  
Mtor Signaling Pathway

Abstract Background The X-linked gene WTX (also called AMER1) has been reported to function as a tumour suppressor gene in Wilms’ tumour. In our previous study, WTX expression was shown to be significantly reduced in gastric cancer (GC), but the function and mechanism associated with WTX loss had yet to be fully elucidated. Methods WTX expression and clinical significance were father analyzed in GC and control normal gastric tissues, and validated in public databases. The candidate pathway which was regulated by WTX during GC progression was searched by KEGG pathway analysis. The miRNA which monitored WTX expression was screened by miRNA microarray. After verified the pathway and miRNA both in vitro and in vivo, the relationship of miRNA, WTX and the downstream pathway were analyzed by Western blot, immunohistochemistry, RT-PCR, Co-immunoprecipitation (Co-IP), and luciferase analyses. Results The results showed that WTX serves as a tumour suppressor gene in GC. The loss of WTX which is associated with the aggressiveness of GC by promoting GC cell proliferation in vitro and high metastasis in vivo. Furthermore, WTX expression was positively correlated with the overall survival of GC patients. Microarray assays, bioinformatics analysis, and verification experiments showed that WTX loss activates the PI3K/AKT/mTOR pathway and promotes GC cell proliferation and invasion. And the aberrant miR-20a-5p upregulation contributes to WTX loss in GC, which stimulates PI3K phosphorylation to activate PI3K/AKT/mTOR signaling pathway and promoted GC progression. Conclusions The results of the present study elucidated the mechanism of GC progression, which is at least partially caused by aberrant miR-20a-5p upregulation leading to the inhibition of WTX expression and PI3K/AKT/mTOR signaling pathway activation. These findings provide a comprehensive understanding of the action of the miR-20a-5p/WTX/PI3K/AKT/mTOR signaling pathway in the progression and metastasis of GC.

tumour suppressor gene and the tobacco industry

The Lancet ◽  
2005 ◽  
Vol 365 (9464) ◽  
pp. 1026-1027
Author(s):  
A BITTON ◽  
M NEUMAN ◽  
J BARNOYA ◽  
S GLANTZ
Keyword(s):  
Tobacco Industry ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor

FOXL2 in adult‐type granulosa cell tumour of the ovary: oncogene or tumour suppressor gene?

2021 ◽  
Author(s):  
Jessica A. Pilsworth ◽  
Anne‐Laure Todeschini ◽  
Samantha J. Neilson ◽  
Dawn R. Cochrane ◽  
Daniel Lai ◽  
...  
Keyword(s):  
Granulosa Cell ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Cell Tumour ◽  
Granulosa Cell Tumour ◽  
Adult Type

scholarly journals Birt–Hogg–Dubé syndrome

2020 ◽  
Vol 29 (157) ◽  
pp. 200042
Author(s):  
Cécile Daccord ◽  
Jean-Marc Good ◽  
Marie-Anne Morren ◽  
Olivier Bonny ◽  
Daniel Hohl ◽  
...  
Keyword(s):  
Index Patient ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Autosomal Dominant Disorder ◽  
Cystic Lung ◽  
Pulmonary Langerhans Cell Histiocytosis ◽  
Renal Tumours ◽  
Pulmonary Cysts ◽  
Chronic Respiratory Insufficiency ◽  
Diagnostic Work

Birt–Hogg–Dubé syndrome (BHD) is a rare inherited autosomal dominant disorder caused by germline mutations in the tumour suppressor gene FLCN, encoding the protein folliculin. Its clinical expression typically includes multiple pulmonary cysts, recurrent spontaneous pneumothoraces, cutaneous fibrofolliculomas and renal tumours of various histological types. BHD has no sex predilection and tends to manifest in the third or fourth decade of life. Multiple bilateral pulmonary cysts are found on chest computed tomography in >80% of patients and more than half experience one or more episodes of pneumothorax. A family history of pneumothorax is an important clue, which suggests the diagnosis of BHD. Unlike other cystic lung diseases such as lymphangioleiomyomatosis and pulmonary Langerhans cell histiocytosis, BHD does not lead to progressive loss of lung function and chronic respiratory insufficiency. Renal tumours affect about 30% of patients during their lifetime, and can be multiple and recurrent. The diagnosis of BHD is based on a combination of genetic, clinical and/or skin histopathological criteria. Management mainly consists of early pleurodesis in the case of pneumothorax, periodic renal imaging for tumour detection, and diagnostic work-up in search of BHD in relatives of the index patient.

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