Knockdown of carbohydrate sulfotransferase 12 decreases the proliferation and mobility of glioblastoma cells via the WNT/β-catenin pathway

Abstract

Glioblastoma (GBM) is a common malignant tumor of the brain. Members of the carbohydrate sulfotransferase (CHST) family are deregulated in various cancer types. However, limited data are available on the role of the members of the CHST family in the development of GBM. The present study aimed to identify the role of significant members of the CHST family in GBM and explore the effects and molecular mechanisms of these significant members on GBM cell proliferation and mobility. In the current study, we demonstrated that CHST12 is the only member of CHST family that is upregulated in GBM tissues and associated with a lower survival rate according to the data obtained from The Cancer Genome Atlas. Similarly, the expression of CHST12 increased in GBM tissues than in adjacent tissues and had an important diagnostic value in distinguishing tumor tissues from adjacent tissues. The high expression of CHST12 indicated a lower overall survival rate, was negatively associated with the Karnofsky Performance Scale score, was positively associated with the KI67 expression rate, and was an independent risk factor for GBM. Knockdown of CHST12 significantly decreased GBM cell proliferation and mobility and inhibited the Wnt/β-catenin pathway. Restoration of β-catenin expression in GBM cells reversed the inhibitory effects of CHST12 knockdown on GBM cell proliferation and mobility. In conclusion, the present study demonstrated that CHST12 may be a novel biomarker for GBM; it regulates GBM cell proliferation and mobility via the WNT/β-catenin pathway.

B7 family member H4 induces epithelial-mesenchymal transition and promotes the proliferation, migration and invasion of colorectal cancer cells

“…Wnt signaling pathway contributes to EMT when extracellular E-cadherin is degraded, β-catenin is able to translocate into the nucleus to induces EMT [ 30–32 ]. The deregulation of Wnt signaling is implicated in the progression of various cancers, such as papillary thyroid cancer [ 33 ], glioblastoma [ 34 ], breast cancer [ 35 ] and liver cancer [ 36 ]. In CRC, TGF-beta1 positively regulates B7-H4 through miR-155/miR-143 axis, thereby promoting cancer cells immune escape [ 37 ].…”

Association between plasma proteome and glioma: A two-sample Mendelian randomization analysis

“…showed that knocking down carbohydrate sulfotransferase 12 can reduce the proliferation and motility of glioblastoma cells through the WNT/βcatenin pathway (24). Tyrosine protein sulfotransferase (TPST) is mainly divided into two subtypes, TPST1 and TPST2 (25).…”

MicorRNA-195 links long non-coding RNA SEMA3B antisense RNA 1 (head to head) and cyclin D1 to regulate the proliferation of glioblastoma cells

“…In conclusion, SEMA3B-AS1 is downregulated in GBM and overexpression of SEMA3B-AS1 can downregulate cyclin D1 and suppress GBM cell proliferation possibly through miR-195. With the increased understanding of the molecular mechanism of GBM [ 26 , 27 ], lncRNAs are expected to be targeted to treat GBM.…”