We are glad to announce that Ramakrishna Mission Vivekananda Educational and Research Institute (RKMVERI) will be conducting a special colloquium on “How Cancer Cells Hide from Immune System : The CMTM6-PD-L1 Story ” on 11 September 2026, 12 Noon at Seminar Hall, Narendrapur Campus.
Speaker : Prof. Prosenjit Sen, Indian Association for the Cultivation of Science (IACS), Kolkata
Co-ordinator: Prof. Abhijit Chakrabarti
Abstract
Cancer cells often use a protein called PD-L1 as a “do not attack me” signal to escape destruction by the immune system. PD-L1 binds to PD-1 on immune cells, particularly T cells, and prevents them from effectively attacking the cancer cell. This study explains how another protein, called CMTM6, helps cancer cells maintain high levels of PD-L1 on their surface. CMTM6 acts like a protective shield for PD-L1, preventing it from being removed and destroyed by the cell’s natural waste-disposal systems, the proteasome and lysosome. CMTM6 does this partly by regulating another protein called PTDSS1, which increases the amount of a particular fat molecule, phosphatidylserine, in the cell membrane. This membrane lipid helps CMTM6 interact strongly with PD-L1 and keeps PD-L1 firmly attached to the surface of the cancer cell. Computer simulations further showed that this interaction can cover important regions of PD-L1, making it more difficult for the cell to chemically modify and destroy it. The study also identified two important amino acids in CMTM6, E175 and N3, which are essential for this protective interaction. When these amino acids were altered, CMTM6 could no longer protect PD-L1 effectively, resulting in increased PD-L1 degradation. In addition, CMTM6 was found to influence chemical modifications of PD-L1 by reducing its phosphorylation and increasing its palmitoylation, changes that help PD-L1 remain on the cell surface. When CMTM6 was removed or its important amino acids were mutated in tumor models, PD-L1 levels decreased, allowing more CD8-positive T cells to enter the tumors and become activated. As a result, tumor growth was reduced, and treatment with anti-PD-1 immunotherapy became significantly more effective. Overall, the study shows that CMTM6 acts like a “bodyguard” for PD-L1, using both membrane lipids and chemical modifications to keep PD-L1 on the surface of cancer cells and help them escape immune attack. Therefore, targeting the CMTM6–PD-L1 interaction or altering the lipid environment of the cancer-cell membrane could provide a new strategy to make cancer cells more visible to the immune system and improve the effectiveness of immunotherapy.
| Faculty/Staff Name | Details |
|---|---|
| Abhijit Chakrabarti (Primary Coordinator) | ARD – Narendrapur Campus |