Pancreatic cancer has a BRL 50481 survival rate of less than 25% at five years after partial pancreaticoduodenectomy and is one of the most aggressive and intractable human malignant tumors. Recent studies have shown that the microenvironment serve a function in the progression of malignant epithelial tumors, thus highlighting the importance of understanding of DOI hydrochloride stromal cells in the prevention of cancer cell aggression and anti-cancer treatment strategies. To understand fully the mechanism driving tumor recurrence, metastasis, and clinical outcome in cancer patients, the role of the tumor microenvironment must be examined. In particular, cancer-associated fibroblasts have been found to serve a crucial function through paracrine interactions with adjacent epithelial cancer cells. Caveolins comprise a family of scaffolding proteins that coat 50 nm to 100 nm plasma membrane invaginations. The Cav family is composed of three isoforms: Cav-1, Cav-2, and Cav- 3. The Cav-1 gene is located in chromosome 7 and includes three exons and two introns. Cav-1 is a structural component of caveolae involved in diverse cellular functions, such as vesicular transport, cholesterol homeostasis, and signal transduction. Despite a growing body of evidence on Cav-1 implication in tumorigenesis, whether Cav-1 serves as a tumor suppressor or as an oncogene remains unclear. These contradictory results are probably derived from the study of malignant epithelial tumors. A new paradigm of ����the autophagic tumor stroma model of cancer metabolism���� was recently introduced to facilitate understanding of the function of tumor microenvironments. In this model, the loss of stromal Cav-1 as a key regulator is a potential therapy target, thus suggesting the prognostic importance of stromal Cav-1. Loss of stromal Cav-1 is the single independent predictor of early breast cancer recurrence and progression. Ayala et al. reported that loss of stromal Cav-1 contributed to the metastatic behavior of prostate cancer cells through a mechanism that involving the upregulation of TGF-b1 and SNCG through Akt activation. Zhao et al. reported that Cav-1 expression level in CAFs predicted gastric cancer outcomes. Karen et al. stated that the loss of stromal Cav-1 expression in malignant melanoma metastases predicted poor survival. Solid tumors are no longer considered simply as clonal expansions of cancer cells. In addition to acquired cell intrinsic properties, tumor initiation and growth are supported by an abundance of parenchymal, inflammatory, and stromal cell types, which infiltrate and surround the tumor. Our findings highlight the importance of an evolving microenvironment and suggest that therapy should target both neoplastic cells and supportive stromal cells.