Subhamoy Pratihar
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Subhamoy Pratihar has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Aleepta Guha Ray
Section of Genetic Medicine, Department of Medicine, The University of Chicago, Chicago, IL, United States
1 shared publication - Arun Bandyopadhyay
Cardiovascular Disease and Respiratory Disorders Laboratory, Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India
1 shared publication - Jahangir Alam
Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, IICB TRUE Campus, CN-6, Sector 5, Salt Lake, Kolkata, 700091, WB, India; Academy of Scientific and Innovative Research (AcSIR), Sector 19, Kamala Nehru Nagar, Ghaziabad, 201002, India
1 shared publication Sudipta Sarkar
School of Applied and Interdisciplinary Sciences, Indian Association for the Cultivation of Sciences, 2A&2B, Raja Subodh Mallick Rd, Jadavpur, Kolkata, 700032, WB, India
1 shared publication- Sudipta Sarkar
Indian Association for the Cultivation of Science
1 shared publication Surajit Sinha
School of Applied and Interdisciplinary Sciences, Indian Association for the Cultivation of Sciences, 2A&2B, Raja Subodh Mallick Rd, Jadavpur, Kolkata, 700032, WB, India
1 shared publication
Latest Publications
- 5 May 2026
- Published by Elsevier in Atherosclerosis
- Vol. 417, 120764
Hepatic GSTM3 deficiency Accelerates Atherosclerosis through redox-driven mitochondrial dysfunction and necroinflammation in Apoe−/− mice
- 5 May 2026
- Published by Elsevier in Atherosclerosis
- Vol. 417, 120764
Hepatic GSTM3 deficiency Accelerates Atherosclerosis through redox-driven mitochondrial dysfunction and necroinflammation in Apoe−/− mice
- Open Access
Cell-Permeable Morpholino Inhibits Programmed Death-Ligand 1 at mRNA Level and Potentiates Antitumor Immunity in Breast Cancer
Morpholino-based ASOs with nuclease-resistant backbone and high sequence specificity could modulate the PD-L1/PD-1 axis to overcome T regulatory cell mediated inhibition but poor cell-permeability limits their clinical applications. Here, we develop a guanidinium-modified cell-permeable morpholino specifically targeting PD-L1 in breast cancer. It suppresses PD-L1 expression through effectively mitigating cytokine induced PD-L1 upregulation and enhancing autophagic flux. Notably, the ASO synergistically with durvalumab (anti-PD-L1 antibody) disrupt, hyperglycosylated PD-L1 by mRNA-level interference and also reduced PD-1⁺ T-cell populations. Importantly, systemic and intra-tumoral administration of ASO demonstrated no abnormalities in cardiac tissues which show no off-target toxicity but it reprogrammed the tumor microenvironment by upregulating inducible nitric-oxide synthase and suppressed regulatory cells, collectively enhancing antitumor immune responses. Together, these findings establish morpholino ASO as a promising targeting therapeutic strategy to overcome tumor-induced immunosuppression, opening new avenues for precision treatment in breast-cancer.
Open AccessCell-Permeable Morpholino Inhibits Programmed Death-Ligand 1 at mRNA Level and Potentiates Antitumor Immunity in Breast Cancer
Morpholino-based ASOs with nuclease-resistant backbone and high sequence specificity could modulate the PD-L1/PD-1 axis to overcome T regulatory cell mediated inhibition but poor cell-permeability limits their clinical applications. Here, we develop a guanidinium-modified cell-permeable morpholino specifically targeting PD-L1 in breast cancer. It suppresses PD-L1 expression through effectively mitigating cytokine induced PD-L1 upregulation and enhancing autophagic flux. Notably, the ASO synergistically with durvalumab (anti-PD-L1 antibody) disrupt, hyperglycosylated PD-L1 by mRNA-level interference and also reduced PD-1⁺ T-cell populations. Importantly, systemic and intra-tumoral administration of ASO demonstrated no abnormalities in cardiac tissues which show no off-target toxicity but it reprogrammed the tumor microenvironment by upregulating inducible nitric-oxide synthase and suppressed regulatory cells, collectively enhancing antitumor immune responses. Together, these findings establish morpholino ASO as a promising targeting therapeutic strategy to overcome tumor-induced immunosuppression, opening new avenues for precision treatment in breast-cancer.