<p>circPDSS1 Stimulates the Development of Colorectal Cancer via Activating the Wnt/β-Catenin Signaling</p>

Abstract

This study aims to illustrate the role of circPDSS1 and the Wnt/β-catenin signaling in the development of colorectal cancer (CRC). Patients and Methods: Cancerous mucosa and normal paracancerous mucosa tissues more than 5 cm away from the tumor were surgically collected from 56 CRC patients. circPDSS1 levels in collected tissues and CRC cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The influence of circPDSS1 on clinical features of CRC patients was analyzed. After knockdown of circPDSS1 in HCT-8 and HCT-116 cells, phenotype changes were examined by Transwell, tube formation and wound healing assay. Western blot and rescue experiments were finally performed to uncover the role of circPDSS1 and the Wnt/β-catenin signaling in the development of CRC. Results: circPDSS1 was upregulated in CRC mucosa tissues than controls. High level of circPDSS1 predicted high rates of lymphatic metastasis and distant metastasis, and poor prognosis in CRC patients. Knockdown of circPDSS1 attenuated migratory ability and angiogenesis in CRC cells. Protein levels of key genes in the Wnt/β-catenin signaling, including β-catenin, GSK-3β, c-Myc, MMP-9 and cyclin D1 were downregulated in CRC cells transfected with sh-circPDSS1. Overexpression of β-catenin reversed the role of circPDSS1 in attenuating migratory ability and angiogenesis in CRC cells. Conclusion: Upregulated circPDSS1 in CRC is closely linked to lymphatic metastasis, distant metastasis and overall survival. It stimulates the migratory ability and angiogenesis in CRC cells via activating the Wnt/β-catenin signaling.

Propofol Suppresses Gastric Cancer Progression by Regulating circPDSS1/miR-1324/SOX4 Axis

“…Fang et al pointed out that circPDSS1 was upregulated in colorectal cancer tissues and circPDSS1 promoted migratory ability and angiogenesis in colorectal cancer cells via activating Wnt/β-catenin signaling. 32 In addition, Yu et al declared that circPDSS1 promoted the development of bladder cancer via downregulation of miR-16. 33 More importantly, Ouyang et al revealed that circPDSS1 was upregulated in GC tissue samples and cell lines, and knockdown of circPDSS1 repressed GC cell proliferation and accelerated apoptosis via sponging miR-186-5p and regulating NEK2.…”

Therapeutic strategies targeting Wnt/β‑catenin signaling for colorectal cancer (Review)

“…Aberrantly expressed ncRNAs have been demonstrated to be associated with cRc tumorigenesis (25,(62)(63)(64)(65)(66)(67). Additionally, the aberrant expression of ncRNAs is correlated to the clinicopathological characteristics of cRc, such as prognosis (68), survival (69,70) and metastasis (1,7,8,62,(71)(72)(73)(74)(75). In the present review, the aberrant expression of ncRNAs and their effects on cRc in the Wnt/β-catenin signaling pathway are presented in Table I (5,7,8,25,36,(62)(63)(64)(65)(66)(67)(68)(69)(70).…”

“…The exact mechanisms of the functional roles of circRNA in CRC remain elusive. Additionally, the upregulation of circRNA-PDSS1 promotes migratory ability and angiogenesis in CRC cells via the upregulation of β-catenin, c-Myc, cyclin D1 and MMP-9, leading to lymphatic metastasis and distant metastasis ( 75 ).…”

Extracellular vesicle‐mediated regulation of tumor angiogenesis— implications for anti‐angiogenesis therapy

“…Up to date, it has been reported that multiple molecules and mechanisms (eg VEGF/ VEGFR2 signalling, 47 MAPK, 48 Notch signalling 49 and Wnt/β‐catenin signalling 50 ) are involved in tumour angiogenesis. Also, accumulating studies find that tumour‐derived EVs contain proteins related to the signalling pathways mentioned above, thus making the EVs a vital role in tumour angiogenesis.…”

“…Up to date, it has been reported that multiple molecules and mechanisms (eg VEGF/ VEGFR2 signalling, 47 MAPK, 48 Notch signalling 49 and Wnt/β-catenin signalling 50 ) are involved in tumour angiogenesis.…”