Oral cancer patients at an advanced stage show poor clinical outcomes. Cancer stem cells (CSCs) within these tumors are able to evade chemo-radiotherapy, leading to the recurrence of disease post-treatment. Our group is investigating the mechanisms involved in the maintenance of CSCs. Whole transcriptome profile was carried out for the CSCs isolated from patient samples which revealed a distinct metabolic rewiring hinting towards new avenues to target CSCs.

Dab2 (Disabled-2 protein) is an adaptor protein and acts as a Wnt inhibitor. This group's finding showed that Dab2 knockout mice showed decreased cell proliferation and stem cells lost their stemness potential. Further, skin-induced tumors using DMBA/TPA application in the Dab2 knock-out skin showed decreased proliferation of the cells, and also, the tumors do not progress into squamous cell carcinoma.

SFRP1 (Secreted frizzled-related protein), a Wnt inhibitor, is downregulated in various human cancers. Cancer stem-like cells isolated from the Sfrp1 knock-out tumors showed higher tumorigenic potential. Molecular profiling on cancer stem cells revealed upregulation of epithelial to mesenchymal transition (EMT) markers, Akt, and also stem cell marker, Sox2. Importantly, inverse co-relation of Sfrp1 and Sox2 was observed in human oral and breast cancer patient samples.

Secretory phospholipase A2 group-IIA (sPLA2-IIA) catalyzes the sn-2 position of glycerophospholipids to yield fatty acids and lysophospholipids. sPLA2-IIA is deregulated in various human cancers. Findings from this laboratory are that sPLA2-IIA knockdown in oral cancer cell lines showed decreased tumorigenic potential through c-Jun/JNK activation. Similarly, sPLA2-IIA knockdown in breast cancer cells and breast cancer stem cells (BCSCs) also showed decreased tumorigenic and metastatic potential.