Suppression of migration and invasion by taraxerol in the triple-negative breast cancer cell line MDA-MB-231 via the ERK/Slug axis.

As one of the triterpene extracts of Taraxacum, a traditional Chinese plant, taraxerol (TRX) exhibits antitumor activity. In this study, we evaluated the effects of TRX on the migration and invasion of MDA-MB-231 cells, analyzed the molecular mechanism through network pharmacology and molecular docking, and finally verified it by in vitro experiments. The results showed that TRX could inhibit the migration and invasion of MDA-MB-231 cells in a time- and concentration-dependent manner, while MAPK3 was the most promising target and could stably combine with TRX. In addition, the relative protein expression levels were detected by Western blot, and we observed that TRX could inhibit the migration and invasion of MDA-MB-231 cells via the ERK/Slug axis. Moreover, an ERK activator (tert-butylhydroquinone, tBHQ) partially reversed the suppressive effect of TRX on MDA-MB-231 cells. In conclusion, TRX inhibited the migration and invasion of MDA-MB-231 cells via the ERK/Slug axis.

[Effects of in vitro PTEN transfection on proliferation of human pancreatic cancer ASPC-1 cells].

OBJECTIVE: To investigate the effect of phosphatase and ensinhomology deleted on chromosome ten (PTEN) on the human pancreatic cancer cell line without or low PTEN expression. METHODS: We selected the lowest PTEN gene expressive pancreatic cancer cell line among the four pancreatic cancer cell lines (Miapaca I, Miapaca II, JF305 and ASPC-1) through RT-PCR assay method, and transfected plasmid (Peak8) inserting PTEN or not in vitro into it by lipofectin. The effect of PTEN transfection on the lowest PTEN gene expressive pancreatic cancer cell line was carried out by flow cytometry, immunohistochemical staining, cloning survival assay, as well as tumorigenicity in nude mice. RESULTS: The lowest PTEN gene expression was found in ASPC-1 cells. PTEN mRNA expression and cloning plating efficiency in the ASPC-1, A-pE and A-pE-P cells were 20.3%, 15.0%, 56.8% and 33.3%, 31.7%, 24.0% respectively. We found that ASPC-1 cells transfected with PTEN exhibited significantly more protein, less vascular endothelial growth factor protein, and non-changed epidermal growth factor receptor protein comparing with vector-transfected cells. The tumor volumes were 202.7 mm(3) and 142.4 mm(3), pre-and post-transfection with significance (P < 0.01) within 5 weeks. CONCLUSIONS: Our findings suggested that PTEN mRNA exhibited the lowest expression in ASPC-1 cell line, exogenous PTEN dramatically inhibits the growth of ASPC-1 cells transfected with PTEN gene in nude mice.

Clinical significance of TGF- beta1 and beta-glucuronidase synchronous detection in human pancreatic cancer.

OBJECTIVE: To investigate the relation of transfer growth factor (TGF-beta1) and beta-glucuronidase (beta-GCD) on the occurrence and progress of pancreatic cancer. METHODS: The expression of TGF-beta1 and beta-GCD in the pancreatic cancer tissue and normal pancreatic tissue was determined synchronously using ABC method of immunohistochemistry. RESULTS: The percentage of TGF-beta1 positive cells was significantly higher in pancreatic cancer tissue (43.8%+/-5.2%) than in adjacent pancreatic tissue (28.7%+/-3.6%, P<0.01). The worse the cancer cells differentiated and lymph nodes metastasis, the more over-expression of TGF-beta1. The percentage of beta-GCD positive cells was also significantly higher in the pancreatic cancer tissue (62.5%+/-4.1%) than in the adjacent pancreatic tissue (33.5%+/-2.8%, P<0.01). The degree of over-expression of beta-GCD was related to the degree of cancer cells differentiation, but not to the lymph nodes metastasis. The expression of TGF-beta1 was significantly correlated with the expression of beta-GCD in pancreatic cancer tissue. CONCLUSIONS: The genesis of pancreatic cancer results from multi-factor, multi-step and multi-gene variation. The synchronous detection of TGF-beta1 and beta-GCD helps to determine the malignant degree of tumors and the prognosis of patients with such disease.

KAI1 gene is differently expressed in papillary and pancreatic cancer: influence on metastasis.

AIM:To compare KAI1 in cancer of papilla of Vater and pancreas to evaluate whether there are differences in biologic behavior which might account for prognosis.METHODS:We compared the expression in 24 papillay and 29 pancreatic cancers using Northern blot analysis, immunochemical assay and in situ hybridization, and investigated whether early diagnosis or molecular differences predict the outcome in these tumor entities.RESULTS:By Northern blot analysis there is no statistical difference of KAI1 levels in normal and cancerous papilla. No association between KAI1 mRNA expression and tumor stage or tumor differentiation was found in the tumors. By immunohistochemical assay, KAI1 staining in cytoplasm of papillary cancer cells was similar to that of normal papillary cells. By in situ hybridization, the results of KAI1 mRNA expression in normal and cancerous papilla were similar to those with immunohistochemical assay. The normal and cancerous pancreas tissues were also analyzed by the methods used in papillary samples.CONCLUSION:Although the biologic roles of KAI1 have not been clarified, our results suggest that KAI1 may restrict the progression of malignant papillary cancer, but its expression might not have any effect on the characteristics of papillary tumor, whereas by the analysis of KAI1 gene, its reduced expression is closely related to the progression and metastases of pancreatic cancer.