Anti-CTNNB1 (mutation T41A) Monoclonal Antibody, clone XH032

Hepatocellular carcinoma (HCC), a common malignant tumor, has been regarded as a leading cause of cancer-related deaths globally. Astragaloside IV (AS-IV) was reported to participate in the regulation of multiple tumors. However, the role of AS-IV in HCC was still unclear in HCC. Bioinformatics analysis and function or mechanism experiments including RT-qPCR, MTT assay, flow cytometry, Western blot, luciferase reporter assay and xeno-grafts assays were applied to investigate the function of AS-IV, miR-150-5p and CTNNB1. We discovered that AS-IV treatment was supposed to significantly increase miR-150-5p level. In addition, AS-IV accelerated cell apoptosis by inducing miR-150-5p in vitro and in vivo. Furthermore, AS-IV increased cell apoptosis rate through reducing beta-catenin level in vitro and in vivo. In detail, AS-IV triggered a decline of Bax and a rise of Bcl-2 in HCC cells and xenograft tissues. In mechanism, we validated the combination between miR-150-5p and CTNNB1. Moreover, miR-150-5p could negatively regulate CTNNB1 level by binding to its3'UTR. Finally, rescue assay demonstrated that CTNNB1 overexpression partially rescued the inhibitive effect on tumor growth and promotive influence on cell apoptosis caused by miR-150-5p amplification. The up-regulation of miR150-5p induced by AS-IV suppressed the progression of HCC by repressing beta-catenin, providing a new molecular target for the utilization of AS-IV In the treatment of HCC.

There is currently no blood-based marker in routine use for endometrial cancer patients. Such a marker could potentially be used for early detection, but it could also help to track tumor recurrence following hysterectomy. This is important, as extravaginal recurrence of endometrial endometrioid adenocarcinoma is usually incurable. This proof-of-principle study was designed to determine if tumor-associated mutations could be detected in cell-free DNA from the peripheral blood of early and late stage endometrial endometrioid carcinoma patients. Approximately 90% of endometrioid carcinomas have at least one mutation in the genes CTNNB1, KRAS, PTEN, or PIK3CA. Using a custom panel targeting 30 hotspot amplicons in these four genes, next-generation sequencing was performed on cell-free DNA extracted from plasma obtained from a peripheral blood draw at the time of hysterectomy and the matching tumor DNA from 48 patients with endometrioid endometrial carcinomas. At least one mutation in the tumor was detected in 45/48 (94%) of patients. Fifteen of 45 patients (33%) had a mutation in the plasma that matched a mutation in the tumor. These same mutations were not detected in the matched negative control buffy coat. Presence of a plasma mutation was significantly associated with advanced stage at hysterectomy, deep myometrial invasion, lymphatic/vascular invasion, and primary tumor size. Detecting a plasma-based mutation was independent of the amount of cell-free DNA isolated from the plasma. Overall, 18% of early stage patients had a mutation detected in the plasma. These results demonstrate that mutations in genes relevant to endometrial cancer can be identified in the peripheral blood of patients at the time of surgery. Future studies can help to determine the post-operative time course of mutation clearance from the peripheral blood and if mutation re-emergence is predictive of recurrence.