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.