Dr. Sangeeta Choudhury

 Dr. Sangeeta Choudhury |Clyto Access

Senior Consultant, Sir Ganga Ram Hospital, India

Speaker

Expertise: Cancer biology, Stem cell biology, Transplantation Immunology, Obesity and Metabolism in Type II diabetes

Biography:

Dr. Sangeeta Choudhury, carried her PhD at Bhabha Atomic Energy Research Centre, (BARC) Mumbai at the Department of Carcinogenesis & Tata Institute of Fundamental Research (TIFR), Mumbai. Presently she is working as a Senior Consultant, Department of Research, Sir Ganga Ram Hospital, India.
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Presentation:

Title: MODULATION OF MUC-1 BY VITAMIN D IN PANCREATIC CANCER

Abstract:

Over the years, pancreatic cancer has been established as a complicated disease with poor prognosis and survival rate. Standard chemotherapeutic agents/drugs have not shown any significant advancement in its regression. Several studies have indicated anti-angiogenesis and blocking the cancerous growth of breast, prostate, lung and colon by micronutrients like vitamin D, E, B12. Although, pancreatic cancer tissue expresses Vitamin D (VitD) receptor, the potential mechanism to exert anti-cancer effect remains underexplored.  
Thus, our study aimed to find out the mechanistic effect caused by the VitD analogue (Calcitirol) in pancreatic cancer cells. Pancreatic cancer cells (PCC lines; MiaPaCa2 and PanC-1) treated with calcitirol for longer duration (24hrs-to-96hrs) showed decreased expression of metastatic phenotype, CXCR4/CCL12, EpCAM/Vimentin along with decreased chemoresistant-MUC-1 expression, although no inhibitory effect was observed on their proliferative capacity. But, addition of Gemcitabine (Gem) to calcitirol-treated PCC lines increased their apoptotic capability than cells treated only with Gem, suggesting that calcitirol treated-PCC cells are susceptible to chemotherapeutic drug. Further, with the emergence of stroma playing a major role in pancreatic cancer, we attempted to elicit the involvement of Vit D in Sonic Hedgehog (SHH) signaling. Enhanced apoptosis was observed when salinomycin (SHH inhibitor) was administered to calcitirol treated-PCC cells. Copy numbers of transcription factors C-myc, SMO, PTCH1, PTCH2, and hypoxia-induced factor (HIF1-α) were observed to show increased expression in treated PCC lines in comparison to untreated cells. 

In conclusion, our experimental evidence postulates a potential role of VitD-analogue, calcitirol modulating the pancreatic tumor-associated MUC-1 within its stromal niche. 

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Related Conferences :

International Conference on Cancer Care and Cure