The small heat shock protein βA-crystallin negatively regulates pancreatic tumorigenesis

Our recent study has shown that βA-crystallin appears to act as a tumor suppressor in pancreas. Here, we analyzed expression patterns of βA-crystallin in the pancreatic tumor tissue and the neighbor normal tissue from 74 pancreatic cancer patients and also pancreatic cancer cell lines. Immunocytochemistry revealed that βA-crystallin was highly expressed in the normal tissue from 56 patients, but barely detectable in the pancreatic tumor tissue. Moreover, a low level of βAcrystallin predicts poor prognosis for patients with pancreatic duct adenocarcinoma (PDAC). In the 12 pancreatic cell lines analyzed, except for Capan-1 and Miapaca-2 where the level of βA-crystallin was about 80% and 65% of that in the control cell line, HPNE, the remaining pancreatic cancer cells have much lower βA-crystallin levels. Overexpression of βA-crystallin in MiaPaca-1 cells lacking endogenous βAcrystallin significantly decreased its tumorigenicity ability as shown in the colony formation and wound healing assays. In contrast, knockdown of βA-crystallin in the Capan-1 cells significantly increased its tumorigenicity ability as demonstrated in the above assays. Together, our results further demonstrate that βA-crystallin negatively regulates pancreatic tumorigenesis and appears to be a prognosis biomarker for PDAC.