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- 저자 : Rajkumar Subramani (검색결과 4 건)
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Radioiodination strategies for carborane compounds
Rajkumar Subramani,Abhinav Bhise,유정수 대한방사성의약품학회 2022 Journal of radiopharmaceuticals and molecular prob Vol.8 No.1
The development of methods for the inert and stable radiohalogenation of targeted radiopharmaceuticals is a prerequisite for real-time diagnosis and therapy using radiohalogenated radiopharmaceuticals. Radiohalogenated carboranes demonstrate superior stability in vivo and versatile applications compared with directly labeled tyrosine analogues or synthetically modified organic compounds. Herein, we focus on the most common approaches for the radioiodination (123I, 124I, 125I, and 131I) of carborane derivatives.
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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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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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Recent progress of enzyme cleavable linker in antibody–drug conjugates: sulfatase and phosphatase
Sushil K. Dwivedi,Abhinav Bhise,Rajkumar Subramani,유정수 대한방사성의약품학회 2021 Journal of radiopharmaceuticals and molecular prob Vol.7 No.1
Recently, antibody–drug conjugates (ADCs) are used to deliver efficient cytotoxic payloads selectively in cancer cells. In the designing of an ADC, the antibody is connected to a toxic payload via a covalent linker, which helps to solubilizes the typical hydrophobic payload as well as stabilizes the linkage over circulation. The development of the linkers for the antibody drug conjugate is still in demand. Initially, the acid, disulfide, and cathepsin-sensitive ADCs attracted considerable attention for the delivery of a potent cytotoxic payload but suffer from instability in human and mouse plasma with a short half-life. In addition, It also suffer from a solubility issue that induces aggregation, which is the major problem in their development. ADCs associated with sulfatase and phosphatase cleavable linker are highly soluble due to the anionic nature of sulfate and phosphate groups. The ADCs also showed high stability in human and mouse plasma. Therefore, to overcome these limitations, sulfatase and phosphatase cleavable linkers were developed. This review focuses on the recently reported advantages of sulfatase and phosphatase cleavable linkers for ADCs.
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