Where the GM2 story
goes next.
Research directions documented through the laboratory and Bose Institute profiles, presented here as a forward-looking research portfolio.
GM2–Hippo–YAP/TAZ
Identify upstream receptors or components linking GM2 to Hippo pathway inactivation, YAP/TAZ nuclear signalling, EMT and metastasis.
Tumour–Stroma Crosstalk
Define how GM2-driven tumour–stromal interactions and cancer-associated fibroblast signatures contribute to metastatic behaviour.
GM2-Synthase Structure
Biochemical and structural characterization of GM2-synthase using molecular, mutational and future high-resolution structural approaches.
Follow the
evidence.
A compact view of the laboratory's scientific trajectory—from gene regulation to the behaviour of the tumour cell and its ecosystem.
Why GM2-synthase rises.
Our work has investigated transcriptional and chromatin mechanisms underlying B4GALNT1/GM2-synthase deregulation in cancer.
GM2 becomes a signalling cue.
GM2-associated membrane signalling engages integrin-linked pathways and the FAK/Src-ERK axis, connecting lipid abundance to malignant cell behaviour.
A lipid can change phenotype.
GM2-driven signalling is linked with EMT, migration, invasion and anchorage-independent growth, providing a mechanistic bridge to metastatic competence.
One lipid. Multiple scales of biology.
Follow the laboratory's central mechanistic thread from gene regulation to tumour-cell signalling, microenvironmental remodelling and metastatic growth.
+ SIGNAL
→ ERK / EGR1
· INVASION
→ TME / CAF
GROWTH
What is established
and what remains open.
The website distinguishes the laboratory's GM2-specific mechanistic findings from broader evidence on ganglioside-mediated tumour-microenvironment effects, while presenting the overall sequence as a mechanistic research model rather than implying that every TME effect has already been proven to be GM2-specific.
GM2-specific evidence
GM2 has been shown to interact with integrin and modulate downstream FAK/Src/ERK signalling, promoting migration and invasion; recent work identifies MEK–ERK–Egr1-dependent EMT as a mechanistic axis.
Gangliosides in the TME
Tumour-derived gangliosides can be shed into the microenvironment and influence immune and myeloid compartments. GM2 has specifically been reported to inhibit macrophage Fc-receptor expression and to affect dendritic-cell function in experimental systems.
The research opportunity
How GM2-driven tumour-cell signalling connects to stromal, vascular and immune remodelling in a living tumour remains an important mechanistic question—and a natural next chapter for tumour glycobiology.
From Membrane Lipids to Oncogenic Programmes
Our research connects glycosphingolipid biology with downstream cell signalling, transcription factors, epigenetic regulation, and aggressive cancer-cell phenotypes.
Genetic Manipulation of Gangliosides
Genetic manipulation of selected gangliosides to define their roles in migration, invasion, anchorage-independent growth and tumour progression.
Downstream Signalling Cascades
Dissecting how GM2 engages downstream signalling programmes, including MEK/ERK/Egr1 and transcriptional pathways linked to aggressive cancer phenotypes.
Chromatin & Enzyme Regulation
Uncovering epigenetic mechanisms regulating GM2-synthase expression, including the Sp1–HDAC1–p300 regulatory axis.
EMT & Metastatic Transition
Understanding how glycolipid-driven changes influence cellular migration, epithelial-mesenchymal transition (EMT), and systemic metastatic behaviour.
Targeted Gene-Editing Tools
Using targeted genetic tools including TALEN-based editing and contemporary gene-regulatory approaches to interrogate causal disease mechanisms.
Biomarkers & Therapy Response
Exploring whether mechanistic insights into tumour-associated glycolipids can reveal reliable biomarkers and novel therapeutic opportunities.
From Kolkata to
global collaborations.
Recent activities include invited lectures, scientific chairing, conference participation and the initiation of a Bose Institute–FAIR/GSI collaboration.
March 2026: visit to FAIR-GSI, Darmstadt, including the lecture “Glycobiology in Tumorigenesis: The GM2 Saga” and initiation of collaboration with Bose Institute.
Invited to chair the “Immunotherapy—Achievements & Future Directions” session at the 2026 annual meeting in Srinagar.
May 2026: invited lecture at BRIC-NIBMG, Kalyani on transcriptional control of the GM2-synthase gene in cancer.
A scientific journey
built around one
lipid.
Selected milestones from the laboratory’s published work, assembled from the existing Tumour Glycobiology Laboratory website.
GM2/GD2-synthase
Targeted editing linked ganglioside synthesis with anchorage-independent growth and anoikis resistance.
Migration
GM2 was shown to mediate tumour-cell migration through integrin-associated signalling.
Epigenetics
Histone H3 acetylation and loss of the Sp1–HDAC1 complex were linked to GM2-synthase de-repression in RCC.
EMT programme
GM2 was reported to induce EMT through a MEK/ERK/Egr1-dependent transcriptional programme.
p300 mechanism
dCas9-targeted proteome profiling revealed p300-mediated reciprocal SMAD/SP1 regulation driving GM2-synthase transcription.
What the animation represents: GM2 is shown as a membrane-associated signalling cue that can influence cancer-cell behaviour through Integrin/FAK/Src and MEK–ERK–Egr1 pathways, while gangliosides released into the extracellular milieu can modulate immune and myeloid components of the tumour microenvironment. The latter is a broader ganglioside effect; the specific contribution of GM2 to TME remodelling remains an active research question.
From a tumour-derived glycolipid to a regulatory network.
The laboratory's recent work connects GM2 abundance to signalling and transcriptional programmes that help explain cancer-cell plasticity and progression.
Why is GM2 high?
What does GM2 do?
plasma membrane → signalling → malignant phenotype → shedding → CAF/TME → metastatic growth. transcriptional deregulation of the GM2-synthase gene increases GM2 production; GM2 accumulates on the tumour-cell membrane, drives pro-tumorigenic signalling and is actively shed into the tumour microenvironment, where gangliosides can modulate immune, myeloid and stromal compartments.
GM2 biosynthesis: ganglioside synthesis proceeds through the secretory pathway: glucosylceramide → lactosylceramide → GM3, followed by Golgi-localized B4GALNT1/GM2-synthase adding GalNAc to GM3 to form GM2; gangliosides are then trafficked to the plasma membrane. The animation is a schematic of this pathway, not a quantitative metabolic map.
In cancer, deregulation of the B4GALNT1 gene encoding GM2-synthase increases GM2-synthase transcription. Our work links this de-repression to altered chromatin regulation, including loss of the Sp1–HDAC1 repressive state; recent work identifies p300-mediated reciprocal regulation of SMAD and SP1 as a driver of GM2-synthase transcription in RCC.
Increased GM2-synthase activity generates more GM2, producing an aberrantly GM2-rich tumour-cell membrane. GM2 is not merely a passive marker: it participates in membrane microdomains and receptor-associated signalling.
Membrane-associated GM2 can engage signalling machinery including integrin-associated FAK/Src and the MEK–ERK–Egr1 axis, promoting EMT-associated changes, migration and invasion.
Tumour cells actively shed gangliosides into the extracellular milieu. Shed gangliosides can influence immune and myeloid compartments and contribute to an immunosuppressive, tumour-supportive microenvironment. The precise GM2-specific contribution to each TME compartment.