CYR61/CCN1 Regulates dCK and CTGF and Causes Gemcitabine-resistant Phenotype in Pancreatic Ductal Adenocarcinoma

Molecular Cancer Therapeutics
Gargi MaitySnigdha Banerjee

Abstract

Pancreatic ductal adenocarcinoma (PDAC) develops extrinsic- and intrinsic-resistant phenotypes to prevent chemotherapies from entering into the cells by promoting desmoplastic reactions (DR) and metabolic malfunctions of the drugs. It is well established that these responses are also associated with pancreatic cancer cells' gemcitabine resistance. However, the mechanism by which these resistant pathways function in the pancreatic cancer cells remains poorly understood. In these studies, we show that CYR61/CCN1 signaling plays a vital role in making pancreatic cancer cells resistant to gemcitabine in vitro and also in a tumor xenograft model. We proved that the catastrophic effect of gemcitabine could significantly be increased in gemcitabine-resistant PDAC cells when CYR61/CCN1 is depleted, while this effect can be suppressed in gemcitabine-sensitive neoplastic cells by treating them with CYR61/CCN1 recombinant protein. Ironically, nontransformed pancreatic cells, which are sensitive to gemcitabine, cannot be resistant to gemcitabine by CYR61/CCN1 protein treatment, showing a unique feature of CYR61/CCN signaling that only influences PDAC cells to become resistant. Furthermore, we demonstrated that CYR61/CCN1 suppresses the exp...Continue Reading

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Citations

Jun 21, 2019·Oncotarget·Snigdha BanerjeeSushanta K Banerjee
Aug 22, 2020·World Journal of Gastroenterology : WJG·Gabriel Benyomo MpillaAsfar Sohail Azmi
Nov 12, 2019·Frontiers in Oncology·Johanna W HellingerCarsten Gründker
Apr 21, 2021·Journal of Cell Communication and Signaling·Herman Yeger, Bernard Perbal

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