We have a suspicion that you are an automated web bot software, not a real user. To keep our site fast for other users, we have slowed down this page. The slowdown will gradually disappear. If you think this is a mistake, please contact us at genome-www@soe.ucsc.edu. Also note that all data for hgGeneGraph can be obtained through our public MySQL server and all our software source code is available and can be installed locally onto your own computer. If you are unsure how to use these resources, do not hesitate to contact us.
UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining
J Med Food 2012, PMID: 22191569

Bitter melon (Momordica charantia) extract suppresses adrenocortical cancer cell proliferation through modulation of the apoptotic pathway, steroidogenesis, and insulin-like growth factor type 1 receptor/RAC-α serine/threonine-protein kinase signaling.

Brennan, Victoria C; Wang, Chiung-Min; Yang, Wei-Hsiung

Adrenocortical carcinomas are rare but present with extremely poor prognosis. One of the approaches to control cancer progression and reduce cancer risk is prevention through diet. Bitter melon is widely consumed as a vegetable and especially as a traditional medicine in many countries. In this study, we have used human and mouse adrenocortical cancer cells as an in vitro model to assess the efficacy of bitter melon extract (BME) as an anticancer agent. The protein concentrations of BME and other extracts were measured before use. First, BME treatment of adrenocortical cancer cells resulted in a significantly dose-dependent decrease in cell proliferation. However, we did not observe an antiproliferative effect in adrenocortical cancer cells treated with extracts from blueberry, zucchini, and acorn squash. Second, apoptosis of adrenocortical cancer cells was accompanied by increased caspase-3 activation and poly(ADP-ribose) polymerase cleavage. BME treatment enhanced cellular tumor antigen p53, cyclin-dependent kinase inhibitor 1A (also called p21), and cyclic AMP-dependent transcription factor-3 levels and inhibited G1/S-specific cyclin D1, D2, and D3, and mitogen-activated protein kinase 8 (also called Janus kinase) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival. Third, BME treatment decreased the key proteins involved in steroidogenesis in adrenocortical cancer cells. BME treatment decreased the level of phosphorylation of cyclin-dependent kinase 7, which is required, at least in part, for steroidogenic factor 1 activation. Finally, we observed that BME treatment significantly reduced the level of insulin-like growth factor 1 receptor and its downstream signaling pathway as evidenced by lower levels of phosphorylated RAC-α serine/threonine-protein kinase. Taken together, these data illustrate the inhibitory effect of bitter melon on cell proliferation of adrenocortical cancer through modulation of diverse mechanisms.

Diseases/Pathways annotated by Medline MESH: Adrenocortical Carcinoma
Document information provided by NCBI PubMed

Text Mining Data

transcription factor-3 ⊣ G1/S-specific cyclin D1: " BME treatment enhanced cellular tumor antigen p53, cyclin dependent kinase inhibitor 1A ( also called p21 ), and cyclic AMP dependent transcription factor-3 levels and inhibited G1/S-specific cyclin D1 , D2, and D3, and mitogen activated protein kinase 8 ( also called Janus kinase ) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival "

transcription factor-3 ⊣ mitogen activated protein kinase 8: " BME treatment enhanced cellular tumor antigen p53, cyclin dependent kinase inhibitor 1A ( also called p21 ), and cyclic AMP dependent transcription factor-3 levels and inhibited G1/S-specific cyclin D1, D2, and D3, and mitogen activated protein kinase 8 ( also called Janus kinase ) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival "

p53 ⊣ G1/S-specific cyclin D1: " BME treatment enhanced cellular tumor antigen p53 , cyclin dependent kinase inhibitor 1A ( also called p21 ), and cyclic AMP dependent transcription factor-3 levels and inhibited G1/S-specific cyclin D1 , D2, and D3, and mitogen activated protein kinase 8 ( also called Janus kinase ) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival "

p53 ⊣ mitogen activated protein kinase 8: " BME treatment enhanced cellular tumor antigen p53 , cyclin dependent kinase inhibitor 1A ( also called p21 ), and cyclic AMP dependent transcription factor-3 levels and inhibited G1/S-specific cyclin D1, D2, and D3, and mitogen activated protein kinase 8 ( also called Janus kinase ) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival "

cyclin dependent kinase ⊣ G1/S-specific cyclin D1: " BME treatment enhanced cellular tumor antigen p53, cyclin dependent kinase inhibitor 1A ( also called p21 ), and cyclic AMP dependent transcription factor-3 levels and inhibited G1/S-specific cyclin D1 , D2, and D3, and mitogen activated protein kinase 8 ( also called Janus kinase ) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival "

cyclin dependent kinase ⊣ mitogen activated protein kinase 8: " BME treatment enhanced cellular tumor antigen p53, cyclin dependent kinase inhibitor 1A ( also called p21 ), and cyclic AMP dependent transcription factor-3 levels and inhibited G1/S-specific cyclin D1, D2, and D3, and mitogen activated protein kinase 8 ( also called Janus kinase ) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival "

cyclin D1 ⊣ cyclin dependent kinase inhibitor 1A: " BME treatment enhanced cellular tumor antigen p53, cyclin dependent kinase inhibitor 1A ( also called p21 ), and cyclic AMP dependent transcription factor-3 levels and inhibited G1/S-specific cyclin D1 , D2, and D3, and mitogen activated protein kinase 8 ( also called Janus kinase ) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival "

cyclin dependent kinase inhibitor 1A ⊣ mitogen activated protein kinase 8: " BME treatment enhanced cellular tumor antigen p53, cyclin dependent kinase inhibitor 1A ( also called p21 ), and cyclic AMP dependent transcription factor-3 levels and inhibited G1/S-specific cyclin D1, D2, and D3, and mitogen activated protein kinase 8 ( also called Janus kinase ) expression, suggesting an additional mechanism involving cell cycle regulation and cell survival "

Manually curated Databases

No curated data.