Anti-SKIL monoclonal antibody, clone 3G7

Colorectal cancer (CRC) is regarded as one of the top ten malignant cancers, which has caused millions of mortalities all over the world. Although advanced therapeutic methods have been employed to treat CRC, the prognosis of CRC patients remains unsatisfactory. Many researchers claimed long noncoding RNAs (lncRNAs) frequently participate in the development of cancers. Small nucleolar RNA host gene 14 (SNHG14) was proved to play roles in various cancers. Nevertheless, neither biological function nor regulatory mechanism of SNHG14 has been explored in CRC. This investigation is aimed at exploring the role of SNHG14 in CRC. The expression of genes including SNHG14, miR-32-5p, and ski-oncogene-like (SKIL) was measured by RT-qPCR assay. 5-Ethynyl-2 '-deoxyuridine (EdU) assay was employed to measure cell proliferation. Cell migration and invasion were evaluated by transwell assay. Western blot assay was performed to test the protein expression. The binding capacity between miR-32-5p and SNHG14 (or SKIL) was explored by luciferase reporter and RNA immunoprecipitation (RIP) assays. SNHG14 expression is upregulated in CRC cells. Moreover, SNHG14 suppression inhibited the proliferation, metastasis, and epithelial-mesenchymal transition (EMT) process in CRC cells. miR-32-5p presented lower expression, which was negatively regulated by SNHG14. SKIL could combine with miR-32-5p. The mRNA and protein expression of SKIL was downregulated by SNHG14 knockdown or miR-32-5p overexpression. At last, the inhibitory effect of SNHG14 suppression on proliferation, metastasis, and EMT process was rescued by SKIL overexpression. SNHG14 regulates CRC progression via miR-32-5p/SKIL axis, providing a novel point in treatment of CRC patients.

A 3 day old infant with persistent severe hypoglycemia was found to have a cystic pancreatic tumor. Cessation of glucose infusion led to severe hypoglycemia. Pancreaticoduodenectomy was performed and revealed an intraductal papillary mucinous neoplasm (IPMN) with high-grade dysplasia. Sequencing of the IPMN revealed a KRAS gene mutation not present in surrounding normal tissues. Deep sequencing of the patient's blood for KRAS mutations showed no evidence of mosaicism. Whole exome sequencing of the blood of the patient and both parents revealed a de novo germline SKIL mutation in the child that was not present in either parent. This suggests a possible role for SKIL in the pathogenesis of pancreatic tumors. Copyright (C) 2014, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.