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RISS 인기검색어
- 검색키워드
- 저자 : Arunkumar Arumugam (검색결과 2 건)
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Arunkumar Arumugam,Ramadevi Subramani,Sushmita Bose Nandy,Daniel Terreros,Alok Kumar Dwivedi,Edward Saltzstein,Rajkumar Lakshmanaswamy 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Growth hormone receptor (GHR) plays a vital role in breast cancer chemoresistance and metastasis but the mechanism is not fully understood. We determined if GHR could be a potential therapeutic target for estrogen receptor negative (ER−ve) breast cancer, which are highly chemoresistant and metastatic. GHR was stably knocked down in ER-ve breast cancer cells and its effect on cell proliferation, metastatic behavior, and chemosensitivity to docetaxel (DT) was assessed. Microarray analysis was performed to identify potential GHR downstream targets involved in chemoresistance. GHR and ATP-binding cassette sub-family G member 2 (ABCG2) overexpression and knockdown studies were performed to investigate the mechanism of GHR-induced chemoresistance. Patient-derived xenografts was used to study the effect of GHR and ABCG2. Immunohistochemical data was used to determine the correlation between GHR, pAKT, pmTOR, and ABCG2 expressions. GHR silencing drastically reduced the chemoresistant and metastatic behavior of ER-ve breast cancer cells and also inhibited AKT/mTOR pathway. In contrast, activation, or overexpression of GHR increased chemoresistance and metastasis by increasing the expression and promoter activity, of ABCG2. Inhibition of JAK2/STAT5 signaling repressed GHR-induced ABCG2 promoter activity and expression. Further, ABCG2 knockdown significantly increased the chemosensitivity. Finally, patient-derived xenograft studies revealed the role of GHR in chemoresistance. Overall, these findings demonstrate that targeting GHR could be a novel therapeutic approach to overcome chemoresistance and associated metastasis in aggressive ER-ve breast cancers.
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Ramadevi Subramani,Rebecca Lopez-Valdez,Alyssa Salcido,Thiyagarajan Boopalan,Arunkumar Arumugam,Sushmita Nandy,Rajkumar Lakshmanaswamy 생화학분자생물학회 2014 Experimental and molecular medicine Vol.46 No.-
Pancreatic cancer is the only major cancer with very low survival rates (1%). It is the fourth leading cause of cancer-relateddeath. Hyperactivated growth hormone receptor (GHR) levels have been shown to increase the risk of cancer in general and thispathway is a master regulator of key cellular functions like proliferation, apoptosis, differentiation, metastasis, etc. However, todate there is no available data on how GHR promotes pancreatic cancer pathogenesis. Here, we used an RNA interferenceapproach targeted to GHR to determine whether targeting GHR is an effective method for controlling pancreatic cancer growthand metastasis. For this, we used an in vitro model system consisting of HPAC and PANC-1 pancreatic cancer cells lines. GHRis upregulated in both of these cell lines and silencing GHR significantly reduced cell proliferation and viability. Inhibition ofGHR also reduced the metastatic potential of pancreatic cancer cells, which was aided through decreased colony-forming abilityand reduced invasiveness. Flow cytometric and western blot analyses revealed the induction of apoptosis in GHR silenced cells. GHR silencing affected phosphatidylinositol 3 kinase/AKT, mitogen extracellular signal-regulated kinase/extracellular signalregulatedkinase, Janus kinase/signal transducers and activators of transcription and mammalian target of rapamycin signaling,as well as, epithelial to mesenchymal transition. Interestingly, silencing GHR also suppressed the expression of insulin receptor-βand cyclo-oxygenease-2. Altogether, GHR silencing controls the growth and metastasis of pancreatic cancer and reveals itsimportance in pancreatic cancer pathogenesis.
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