Major Research Area
Cancer Biology and Cancer Stem Biology with the specialization of Genomics and Proteomics
About Our Research
Presently, Our research group is focusing on understanding the molecular mechanism of Breast cancer stem cells (CD44+/CD24⁻ phenotype) development in the presence of chemotherapeutic drugs by establishing few chemotherapeutic drug-resistant cell lines. The other objective is also to delineate the mechanisms and the cross talk between the Tumor Associated Macrophage (TAMs) when co-infiltrated with breast cancer cells.
Mechanisms of chemoresistance in cancer stem cells
A major problem in cancer treatment is the development of drug resistance. Recent studies implicate a role for cancer stem cell population in their resistance to various chemotherapeutic drugs. Our primary aim concerning cancer stem cells is whether this CSC population actually expands and leads to metastasis during drug therapy. This phenomenon of drug resistance may be result, in part, due to the high level expression of MDR and ATP-binding cassette transporters. However, the relationship between exposure of chemotherapeutic agents and the expansion of drug-resistant cancer stem cell populations has not been fully explored. We also expanded our investigation to proteomic study and trying to understand the proteome level dysregulation of breast cancer stem cells in drug resistant cells. Further, investigation required for underlying the molecular mechanism to activation cancer stem cell in cancer cells through chemotherapeutic drugs.
Tumor Associated Macrophage (TAMs)
The second objective is that, to assess the efficiency of tumor associated macrophage (TAMs) induces the cancer stem cell in cancer cell population. Recent studies confirmed the cancer cells get adopted for our own immune cell such as, macrophage, dendritic cells, and NK cell. Initially, we standardized protocol for differentiation of Tumor Associated Macrophage from THP 1 monocytes cell line. Previous report has been revealed the production of growth factors, chemokines and cytokines in TAMs. Further, we co-infiltrate the TAMs and also added the TAMs cultured media into breast cancer cell line. As we expected, almost 30% increase in the cancer stem cell population (CD44+/CD24⁻) was observed in breast cancer cell lines in both conditions. The increase in cancer stem cell population could be triggered by various growth factors, chemokines and cytokines present in the culture media. This result was evidenced by RT PCR analysis; it shows the increased expression of stemness gene. Our results clear that the cross talks between TAMs and cancer cells. Further, we are extended our investigation to understand the stemness activation mechanism in TAMs co-infiltrated cancer cell lines.